The relationship between an invertebrate and another organism (the host), one of which lives at the expense of the other. Traditionally excluded from definition of parasites are pathogenic BACTERIA; FUNGI; VIRUSES; and PLANTS; though they may live parasitically.
A phylum of unicellular parasitic EUKARYOTES characterized by the presence of complex apical organelles generally consisting of a conoid that aids in penetrating host cells, rhoptries that possibly secrete a proteolytic enzyme, and subpellicular microtubules that may be related to motility.
A genus of protozoa parasitic to birds and mammals. T. gondii is one of the most common infectious pathogenic animal parasites of man.
Invertebrate organisms that live on or in another organism (the host), and benefit at the expense of the other. Traditionally excluded from definition of parasites are pathogenic BACTERIA; FUNGI; VIRUSES; and PLANTS; though they may live parasitically.
A species of coccidian protozoa that mainly infects domestic poultry.
Proteins found in any species of protozoan.
A group of three related eukaryotic phyla whose members possess an alveolar membrane system, consisting of flattened membrane-bound sacs lying beneath the outer cell membrane.
Infections with unicellular organisms formerly members of the subkingdom Protozoa.
The complete genetic complement contained in a set of CHROMOSOMES in a protozoan.
A species of protozoa that is the causal agent of falciparum malaria (MALARIA, FALCIPARUM). It is most prevalent in the tropics and subtropics.
A protozoan parasite causing tropical theileriasis in cattle. It is transmitted by ticks of the Hyalomma genus.
A species of parasitic protozoa that infects humans and most domestic mammals. Its oocysts measure five microns in diameter. These organisms exhibit alternating cycles of sexual and asexual reproduction.
A genus of protozoa found in reptiles, birds, and mammals, including humans. This heteroxenous parasite produces muscle cysts in intermediate hosts such as domestic herbivores (cattle, sheep, pigs) and rodents. Final hosts are predators such as dogs, cats, and man.
A genus of protozoan parasites of the subclass COCCIDIA. Its species are parasitic in dogs, cattle, goats, and sheep, among others. N. caninum, a species that mainly infects dogs, is intracellular in neural and other cells of the body, multiplies by endodyogeny, has no parasitophorous vacuole, and has numerous rhoptries. It is known to cause lesions in many tissues, especially the brain and spinal cord as well as abortion in the expectant mother.
A genus of tick-borne protozoa parasitic in the lymphocytes, erythrocytes, and endothelial cells of mammals. Its organisms multiply asexually and then invade erythrocytes, where they undergo no further reproduction until ingested by a transmitting tick.
The acquired form of infection by Toxoplasma gondii in animals and man.
A genus of protozoan parasites of the subclass COCCIDIA. Various species are parasitic in the epithelial cells of the liver and intestines of man and other animals.
The functional hereditary units of protozoa.
Self-replicating cytoplasmic organelles of plant and algal cells that contain pigments and may synthesize and accumulate various substances. PLASTID GENOMES are used in phylogenetic studies.
Uninuclear cells or a stage in the life cycle of sporozoan protozoa. Merozoites, released from ruptured multinucleate SCHIZONTS, enter the blood stream and infect the ERYTHROCYTES.
Specific particles of membrane-bound organized living substances present in eukaryotic cells, such as the MITOCHONDRIA; the GOLGI APPARATUS; ENDOPLASMIC RETICULUM; LYSOSOMES; PLASTIDS; and VACUOLES.
The product of meiotic division of zygotes in parasitic protozoa comprising haploid cells. These infective cells invade the host and undergo asexual reproduction producing MEROZOITES (or other forms) and ultimately gametocytes.
Infection of the striated muscle of mammals by parasites of the genus SARCOCYSTIS. Disease symptoms such as vomiting, diarrhea, muscle weakness, and paralysis are produced by sarcocystin, a toxin produced by the organism.
Deoxyribonucleic acid that makes up the genetic material of protozoa.
A genus of protozoa that comprise the malaria parasites of mammals. Four species infect humans (although occasional infections with primate malarias may occur). These are PLASMODIUM FALCIPARUM; PLASMODIUM MALARIAE; PLASMODIUM OVALE, and PLASMODIUM VIVAX. Species causing infection in vertebrates other than man include: PLASMODIUM BERGHEI; PLASMODIUM CHABAUDI; P. vinckei, and PLASMODIUM YOELII in rodents; P. brasilianum, PLASMODIUM CYNOMOLGI; and PLASMODIUM KNOWLESI in monkeys; and PLASMODIUM GALLINACEUM in chickens.
Protozoan infection found in animals and man. It is caused by several different genera of COCCIDIA.
Non-photosynthetic plastids derived from RED ALGAE endosymbionts. They are found in species of the phylum APICOMPLEXA including PLASMODIUM MALARAIAE.
Zygote-containing cysts of sporozoan protozoa. Further development in an oocyst produces small individual infective organisms called SPOROZOITES. Then, depending on the genus, the entire oocyst is called a sporocyst or the oocyst contains multiple sporocysts encapsulating the sporozoites.
Substances that are destructive to protozoans.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Any part or derivative of any protozoan that elicits immunity; malaria (Plasmodium) and trypanosome antigens are presently the most frequently encountered.
A protozoan parasite that is the etiologic agent of East Coast fever (THEILERIASIS). Transmission is by ticks of the Physicephalus and Hyalomma genera.
A protozoan parasite of rodents transmitted by the mosquito Anopheles dureni.
Multinucleate cells or a stage in the development of sporozoan protozoa. It is exemplified by the life cycle of PLASMODIUM FALCIPARUM in the MALARIA infection cycle.
The continuous sequence of changes undergone by living organisms during the post-embryonic developmental process, such as metamorphosis in insects and amphibians. This includes the developmental stages of apicomplexans such as the malarial parasite, PLASMODIUM FALCIPARUM.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Infection of cattle, sheep, or goats with protozoa of the genus THEILERIA. This infection results in an acute or chronic febrile condition.
Measure of the number of the PARASITES present in a host organism.
Drugs used to treat or prevent parasitic infections.
The relationships of groups of organisms as reflected by their genetic makeup.
A genus of tick-borne protozoan parasites that infests the red blood cells of mammals, including humans. There are many recognized species, and the distribution is world-wide.
A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.
A genus of TICKS, in the family IXODIDAE, widespread in Africa. Members of the genus include many important vectors of animal and human pathogens.
Red blood cells. Mature erythrocytes are non-nucleated, biconcave disks containing HEMOGLOBIN whose function is to transport OXYGEN.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
The arrangement of two or more amino acid or base sequences from an organism or organisms in such a way as to align areas of the sequences sharing common properties. The degree of relatedness or homology between the sequences is predicted computationally or statistically based on weights assigned to the elements aligned between the sequences. This in turn can serve as a potential indicator of the genetic relatedness between the organisms.
Infections or infestations with parasitic organisms. The infestation may be experimental or veterinary.
Malaria caused by PLASMODIUM FALCIPARUM. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations.
Acquired infection of non-human animals by organisms of the genus TOXOPLASMA.
Determination of parasite eggs in feces.
A surface protein found on Plasmodium species which induces a T-cell response. The antigen is polymorphic, sharing amino acid sequence homology among PLASMODIUM FALCIPARUM; PLASMODIUM CHABAUDI; PLASMODIUM VIVAX; and PLASMODIUM YOELII.
Proteases which use a metal, normally ZINC, in the catalytic mechanism. This group of enzymes is inactivated by metal CHELATORS.
Meissner M, Schlüter D, Soldati D (October 2002). "Role of Toxoplasma gondii myosin A in powering parasite gliding and host ... is more closely related to the gregarines than to coccidia as shown by phylogenetic analysis of apicomplexan parasites inferred ... within their hosts. Merogony may be intracellular or extracellular depending on the species. DNA studies suggest the ... Valigurová, Andrea; Koudela, Břetislav (August 2008). "Morphological analysis of the cellular interactions between the ...
Intracellular parasites typically rely on a third organism, a vector, to transmit the parasite between hosts.[1][3] Rather than ... Since these parasites derive nourishment from their host, this symbiotic interaction is often harmful to the host. Parasites ... Malaria, caused by the apicomplexan parasite Plasmodium falciparum, is an intracellular endoparasite. This parasite relies on a ... Intercellular parasites live in spaces within the host e.g. the alimentary canal, whereas intracellular parasites live in cells ...
The parasite's survival is dependent on a balance between host survival and parasite proliferation. T. gondii achieves this ... Upon infection, the parasites persist as intraneuronal cysts in the central nervous system (CNS) for the lifetime of the host ( ... The intracellular parasite can persist lifelong in the CNS within neurons modifying their function and structure, thus leading ... Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii, an apicomplexan. Infections with toxoplasmosis usually cause ...
However, the parasite's lifecycle begins and completes only when the parasite is passed to a feline host, the only host within ... The parasites first invade cells in and surrounding the intestinal epithelium, and inside these cells, the parasites ... to live indoors and to be neutered or spayed to decrease stray cat populations and to reduce intermediate host interactions. ... Lesions discovered in her brain and eye tissue were found to have both free and intracellular T. gondii'. Infected tissue from ...
37,0 37,1 37,2 «Host cell autophagy is induced by Toxoplasma gondii and contributes to parasite growth»։ The Journal of ... Upon infection, the parasites persist as intraneuronal cysts in the central nervous system (CNS) for the lifetime of the host ( ... The intracellular parasite can persist lifelong in the CNS within neurons modifying their function and structure, thus leading ... Louis M Weiss, Kami Kim (28 April 2011)։ Toxoplasma gondii: The Model Apicomplexan. Perspectives and Methods։ Academic Press։ ...
Apicomplexan pathogens are obligate intracellular parasites. To enter cells, they must bind with high affinity to host cell ... also inhibit invasion suggests that shedding is required to disengage binding interactions between the parasite and host cell ... Apicomplexan rhomboids have a potential role in microneme protein cleavage during host cell invasion. Int. J. Parasitol. 35:747 ... Apicomplexan parasites possess several rhomboid-like genes (Dowse and Soldati, 2005). T. gondii has six, of which three ( ...
... during host-pathogen interactions, as the battle for nutrients might determine the outcome of an infection. To a... ... an innate cellular defence mechanism against intracellular bacteria? Curr Opin Immunol. 2019 Jun 24;60:117-123 Authors: Escoll ... The surface antigens of apicomplexan parasites function as attachment and invasion in host-parasite interaction. Meanwhile, ... In turn, infection by intracellular bacteria provokes metabolic alterations of the host cell that benefit the pathogen. Here, ...
Apicomplexa parasites share a unique invasion mechanism involving a tight interaction between the host cell and the parasite ... Obligate intracellular Apicomplexa parasites share a unique invasion mechanism involving a tight interaction between the host ... The RON2-AMA1 interaction is a critical step in moving junction-dependent invasion by apicomplexan parasites PLoS Pathog. 2011 ... Here we show that RON2 is inserted as an integral membrane protein in the host cell and, using several interaction assays with ...
T. gondii is an obligate intracellular protozoan parasite of the phylum Apicomplexan (of which the causative agent of malaria, ... Knowledge pertaining to the host-parasite interaction could be bolstered by developing a system to specifically label parasite ... Tg-MetRSNLL parasites stained brightly with Alexa Fluor 594 in the parasite cytoplasm, while WT T. gondii parasites exposed to ... Such a system could be extremely useful to study the interaction between the human parasite Toxoplasma gondii and its host. ...
... are closely related obligatory intracellular apicomplexan parasites that invade and multiply in almost all mammalian host cells ... To fully understand these biological differences, the host-parasite interactions of these parasites have been investigated in ... TgGRA2 was successfully purified by HPLC and attempts have been made to study its role in host-parasite interactions using a ... A comparison of host-parasite interactions between Toxoplasma gondii and Neospora caninum ...
Host-pathogen interaction, Bioinformatics. Introduction. Toxoplasma gondii is an obligate intracellular Apicomplexan parasite ... Toxoplasma gondii: purine synthesis and salvage in mutant host cells and parasites. Exp Parasitol. 1982;53(1):77-86. [PubMed] ... Modulation of the host cell proteome by the intracellular apicomplexan parasite Toxoplasma gondii. Infect Immun. 2008;76(2):828 ... As an intracellular pathogen, the interplay between the parasite and host cell is likely to have an impact on all aspects of ...
Interestingly, two intracellular apicomplexan parasites, Toxoplasma gondii and Theleria, have been shown to upregulate ... 2014 Hijacking of host cellular functions by an intracellular parasite, the microsporidian Anncaliia algerae. PLoS One 9: ... Microsporidia Intracellular Development Relies on Myc Interaction Network Transcription Factors in the Host. *Michael R. Botts1 ... 2010 Microsporidia: a model for minimal parasite-host interactions. Curr. Opin. Microbiol. 13: 443-449. ...
Interestingly, two intracellular apicomplexan parasites, Toxoplasma gondii and Theleria, have been shown to upregulate ... 2014 Hijacking of host cellular functions by an intracellular parasite, the microsporidian Anncaliia algerae. PLoS One 9: ... Microsporidia Intracellular Development Relies on Myc Interaction Network Transcription Factors in the Host. Michael R. Botts, ... Microsporidia Intracellular Development Relies on Myc Interaction Network Transcription Factors in the Host. Michael R. Botts, ...
... a large and highly successful phylum of intracellular parasites. Invasion of host cells allows apicomplexan parasites access to ... a rich source of nutrients in a niche that is largely protected from host defenses. All Apicomplexa ad … ... The malaria parasite is the most important member of the Apicomplexa, ... Host-Parasite Interactions * Humans * Malaria / blood * Malaria / parasitology* * Models, Biological * Molecular Motor Proteins ...
It is important to investigate the involvement of mosquitoes, frogs and parasites in this interaction in order to understand ... The reciprocal nature of this relationship is exploited by various blood parasites that use mechanical, salivary or trophic ... reciprocal trophic interaction. Instead of a one-way, predator-prey relationship, there is a cyclical dance of avoidance and ... The relationship between mosquitoes and their amphibian hosts is a unique, ...
This months Genome Watch explores apicomplexan adaptation to parasitism. ... This months Genome Watch explores apicomplexan adaptation to parasitism. ... suggesting that these genes might have emerged in the context of host-parasite interactions. ... Chromerid genomes reveal the evolutionary path from photosynthetic algae to obligate intracellular parasites. eLife 4, e06974 ( ...
... characterized and compared to the TRAP sequences of related apicomplexan parasites. The functional domain of BoTRAP2 was ... IFA showed that BoTRAP2 is mainly localized on the apical end of parasites by rabbit anti-rBoTRAP2-1 polyclonal serum. The ... Various TRAP proteins have been identified in apicomplexan protozoans, but there have been few reports about TRAP proteins in ... in the sporozoite of Plasmodium falciparum and TRAP family proteins are secreted by micronemes and transported to the parasite ...
... biosynthesis-related processes and interspecies interaction. These findings should increase knowledge of the mouse brain ... biosynthesis-related processes and interspecies interaction. These findings should increase knowledge of the mouse brain ... Host-parasite interactome analysis showed that some DETs were involved in immune signaling, metabolism, ... Host-parasite interactome analysis showed that some DETs were involved in immune signaling, metabolism, ...
Host cell infection by apicomplexan parasites plays an essential role in lifecycle progression for these obligate intracellular ... the organising interface between parasite and host cell during entry. Formation of this structure is not, however, shared ... A local H(2)O(2)/myeloperoxidase interaction within wound-recruited neutrophils was demonstrated. These data demonstrate that ... When linked to surface-bound adhesins, this force is passaged to the cell posterior, propelling the parasite forwards. Gliding ...
Calcium ions, through various calcium-dependent protein kinases (CDPKs), regulate key events in parasite growth and development ... including protein secretion, movement, differentiation, and invasion of and escape from host cells. In this study, we ... An interaction between EtSerpin and EtCDPK4 was identified that may contribute to the invasion and development of E. tenella in ... Eimeria tenella is an obligate intracellular apicomplexan protozoan parasite that has a complex life-cycle. ...
Cell Host & Microbe 8:208-18. PMID 20709297.. *Chandramohandas R et al (2009) Apicomplexan parasites co-opt host calpains to ... Genetic Analysis of Parasite Biology and Host-Pathogen Interactions. The ability to saturate the T. gondii genome by ... modulation of host cell activities, and establishment of the unique intracellular niche in which parasites reside. We are also ... Comparative genomics of the apicomplexan parasites Toxoplasma gondii and Neospora caninum: Coccidia differing in host range and ...
This article presents the ultrastructural dynamics of host cell invasion and intracellular survival of Besnoitia besnoiti. Key ... The parasites can be maintained continuously in vitro in a variety of mammalian cell lines and their requirements for growth ... Both forms are invasive and possess typical apicomplexan structures; a three-layered pellicle, conoid, polar ring, microtubules ... The Ultrastructural Dynamics of Parasite-Host Cell Interactions as demonstrated in Besnoitia besnoiti (Apicomplexa, Protozoa): ...
TgATG8 is crucial for normal replication of the parasite inside its host cell. Seemingly unrelated to the catabolic autophagy ... mainly in model organisms such as yeasts but remains poorly characterized in phylogenetically distant apicomplexan parasites. ... Intriguingly, in T. gondii, ATG8 localizes to the apicoplast under normal intracellular growth conditions. The apicoplast is a ... loss of TgATG8 led to abnormal segregation of the apicoplast into the progeny because of a loss of physical interactions of the ...
... overall prevalence of a parasite within a given host species nevertheless varies over space and time. ... 2008) A photosynthetic alveolate closely related to apicomplexan parasites. Nature 451:959-963. ... 1990) Symbiosis within a symbiosis: Intracellular bacteria in the endosymbiotic protist Nephromyces. Mar Biol 107:291-296. ... offers a particularly striking example of the evolutionary malleability of interaction outcomes in many symbiotic associations ...
Molecular Mechanisms of Parasite Invasion von - Englische E-Books aus der Kategorie Medizin günstig bei kaufen & ... For most of the parasites discussed here the ability to penetrate biological barriers and/or to establish intracellular ... Role of the gp85/Trans-Sialidase Superfamily of Glycoproteins in the Interaction of Trypanosoma cruzi with Host Structures 58 ... Current and Emerging Approaches to Studying Invasion in Apicomplexan Parasites 1 Jeffrey Mital and Gary E. Ward SECTION II: ...
RESULTS: Research on the replicating forms of Cryptosporidium parasites and their interaction with the host cell remains ... The comparison of the combined host-parasite transcriptome reveals that C. parvum gene expression is less diverse than the host ... Due to the intracellular location of meronts and later life-cycle stages, oocyst and sporozoites are the only forms of the ... BACKGROUND: Human cryptosporidiosis is caused primarily by two species of apicomplexan protozoa, Cryptosporidium parvum and C. ...
Host cell parasite interactions in babesiosis Babesiosis of domestic animals and man. Ristic M. 1988 53 69 CRC Press, Inc. Boca ... Apicomplexan parasites in the generaBabesia and Plasmodium invade and replicate within erythrocytes, resulting in, respectively ... During this intracellular replicative cycle, the host erythrocyte membrane is altered (8). Changes required for intracellular ... by parasite modifications of host proteins (6). Importantly, both parasite-encoded proteins and modified host proteins may ...
Toxoplasma gondii is an intracellular Apicomplexan parasite and a causative agent of toxoplasmosis in human. It causes ... T. gondii invades the host cell by forming a moving junction (MJ) complex. This complex formation is initiated by ... Chorioretinitis , Drug Design , Encephalitis , Humans , Hydrophobic and Hydrophilic Interactions , Machine Learning , Membranes ... Molecular Docking Simulation , Molecular Dynamics Simulation , Neck , Parasites , Pliability , Toxoplasma , Toxoplasmosis , ...
Toxoplasma Gondii Host Interactions A Story of Immune Attack and Parasite Counterattack Book Description : Toxoplasma gondii is ... Toxoplasma gondii is an obligate, intracellular parasite of the Apicomplexan phylum that is able to infect nearly all warm- ... These experiments made use of a targeted disruption of the ROP16 locus in Type I parasites to identify ROP16-dependent ... Toxoplasma Gondii Host Interactions A Story of Immune Attack and Parasite Counterattack. *Author : Jeroen P. J. Saeij ...
... are conserved in plants and apicomplexan parasites. In Toxoplasma gondii, TgCDPK3 regulates parasite egress from the host cell ... and Toxoplasma gondii are obligate intracellular apicomplexan parasites that rapidly invade and extensively modify host cells. ... Our method provides a new avenue for noninvasive monitoring of host-microbiota interaction dynamics via host-produced proteins ... which is only conserved in Plasmodium and related Apicomplexan parasites and localizes to the parasite food vacuole. Targeting ...
... differentiation and antibody secretion are processes carefully orchestrated by a complex network of intracellular signaling ... The surface antigens of apicomplexan parasites function as attachment and invasion in host-parasite interaction. Meanwhile, ... Emerging evidence suggests that shifts in available fuel sources and intracellular metabolite concentrations profoundly impact ... host immune response is triggered as a result of parasitic invasion. Immunogenicity and potency as a vaccinal candidate antigen ...
Recent knowledge of host cell-parasite interactions and of parasite virulence has brought new insights into the comprehension ... is a conserved transmembrane adhesin of apicomplexan parasites that plays an important role in host-cell invasion. Toxoplasma ... This obligate intracellular parasite was identified early as a pathogen responsible for congenital infection, but its clinical ... Which roles for autophagy in Toxoplasma gondii and related apicomplexan parasites? Besteiro S. Source. DIMNP, UMR5235 CNRS, ...
RESULTS: Research on the replicating forms of Cryptosporidium parasites and their interaction with the host cell remains ... The comparison of the combined host-parasite transcriptome reveals that C. parvum gene expression is less diverse than the host ... Due to the intracellular location of meronts and later life-cycle stages, oocyst and sporozoites are the only forms of the ... BACKGROUND: Human cryptosporidiosis is caused primarily by two species of apicomplexan protozoa, Cryptosporidium parvum and C. ...
These observations indicate that Laz can serve as an important tool in the study of host-pathogen interactions and is worthy of ... an apicomplexan parasite that causes opportunistic infection in immunocompromised individuals. We demonstrate that the ... exhibits a remarkable ability to impede invasion of a number of diverse intracellular pathogens, including the human AIDS virus ... These observations indicate that Laz can serve as an important tool in the study of host-pathogen interactions and is worthy of ...
Metabolism; apicomplexan genomics; genomics of apicomplexan parasites; host cell modulation; host invasion; parasite genomics; ... ApiAP2; apicomplexan parasites; differentiation; gene expression; intracellular parasites; transcription. PMID:. 28317026. ... Here we describe the pathways of host-parasite interaction at the parasitophorous vacuole employed by Toxoplasma and host, ... gondiiIMPORTANCE Apicomplexan parasites such as Toxoplasma and Plasmodium are obligate intracellular parasites that require the ...
  • A distinct mode of shedding has been observed in the related apicomplexan Toxoplasma gondii . (
  • Our studies were performed both in Toxoplasma gondii and Plasmodium falciparum and although AMA1 and RON2 proteins have diverged between Apicomplexa species, we show an intra-species conservation of their interaction. (
  • Toxoplasma gondii and Neospora caninum are closely related obligatory intracellular apicomplexan parasites that invade and multiply in almost all mammalian host cells. (
  • Toxoplasma gondii is an obligate intracellular protozoan parasite that is capable of causing severe disease in immunocompromised humans. (
  • Ocular toxoplasmosis, which is caused by the protozoan parasite Toxoplasma gondii , is the leading cause of retinochoroiditis. (
  • Toxoplasma is an obligate intracellular pathogen that replicates within a parasitophorous vacuole. (
  • The mechanisms by which Toxoplasma grows within its host cell, encysts, and interacts with the host's immune system are important questions. (
  • Toxoplasma gondii is an obligate intracellular Apicomplexan parasite that can infect a wide range of warm-blooded animals including humans [ 1 ]. (
  • 2) Toxoplasma has an extremely wide host cell tropism that includes most nucleated cells. (
  • 3) In humans and other intermediate hosts, Toxoplasma develops into a chronic infection that cannot be eliminated by the host's immune response or by currently used drugs. (
  • These technologies and approaches have been instrumental in increasing our understanding of Toxoplasma replication within its host cell, bradyzoite development, and virulence mechanisms. (
  • Apicomplexa is a phylum of unicellular eukaryotes with specialized intracellular parasites, including more than 5000 species, some of which are clinically important pathogens such as Plasmodium , Toxoplasma gondii , Cryptosporidium , Eimeria , Coccidia , Neospora caninum , Babesia and others, which pose great harm to animal husbandry and public health. (
  • Toxoplasma , and many other species of medical and veterinary importance its iconic representatives, the protistan phylum Apicomplexa has long been defined as a group composed entirely of parasites and pathogens. (
  • For most of the parasites discussed here (Plasmodium falciparum, Toxoplasma gondii, Cryptosporidium parvum, Trypanosoma cruzi and Leishmania spp. (
  • Toxoplasma gondii is an intracellular Apicomplexan parasite and a causative agent of toxoplasmosis in human. (
  • Upon infection with the obligate intracellular parasite Toxoplasma gondii, fast replicating tachyzoites infect a broad spectrum of host cells including neurons. (
  • Detailed immunohistochemistry showed that in infected neurons not only parasitic cysts but also the host cell cytoplasm and some axons stained positive for Toxoplasma antigen suggesting that parasitic proteins might directly interfere with neuronal function. (
  • Here we report that azurin and an azurin-like protein (Laz) from gonococci/meningococci have activity against Toxoplasma, an apicomplexan parasite that causes opportunistic infection in immunocompromised individuals. (
  • We demonstrate that the mechanism of action for Laz involves interfering with the ability of Toxoplasma to adhere to host cells. (
  • Collectively, our data show that Toxoplasma adhesion can be significantly impaired by Laz, and to some extent by azurin, via interactions with SAG1. (
  • Here, we show that the apicomplexan parasites Toxoplasma gondii and Plasmodium berghei, an opportunistic human pathogen and a rodent malaria agent, respectively, produce cytokinins via a biosynthetic pathway similar to that in plants. (
  • Toxoplasma gondii , an important human parasite, has an array of 22 regularly spaced cortical microtubules stemming from a hypothesized organizing center, the apical polar ring. (
  • The parasitophorous vacuole is a unique replicative niche for apicomplexan parasites, including Toxoplasma gondii. (
  • Toxoplasma secretes numerous proteins to modify the forming vacuole, enable nutrient uptake, and set up mechanisms of host subversion. (
  • Here we describe the pathways of host-parasite interaction at the parasitophorous vacuole employed by Toxoplasma and host, leading to the intricate balance of host defence versus parasite survival. (
  • The Apicomplexa phylum includes many parasites that are relevant to human (such as Plasmodium and Toxoplasma ) and veterinary (such as Babesia , Eimeria , and Neospora ) health. (
  • the parasite is closely related to toxoplasma gondii, but the two species are antigenically distinct. (
  • Toxoplasma gondii is an obligate intracellular parasite in the phylum Apicomplexa that causes severe central nervous system disorders of immunocompromised (AIDS/transplant/lymphoma) individuals and birth defects to congenitally infected neonates worldwide. (
  • In addition to being a globally important pathogen, Toxoplasma also serves as a model system for studying Apicomplexan parasites which cause a number of diseases of medical and veterinary importance including Plasmodium falciparum, the causative agent of malaria which kills 1-2 million people each year. (
  • Nadipuram Santhosh M, Kim Elliot W, Vashisht Ajay A, Lin Andrew H, Bell Hannah N, Coppens Isabelle, Wohlschlegel James A, Bradley Peter J In Vivo Biotinylation of the Toxoplasma Parasitophorous Vacuole Reveals Novel Dense Granule Proteins Important for Parasite Growth and Pathogenesis. (
  • Kim Elliot W, Nadipuram Santhosh M, Tetlow Ashley L, Barshop William D, Liu Philip T, Wohlschlegel James A, Bradley Peter J The Rhoptry Pseudokinase ROP54 Modulates Toxoplasma gondii Virulence and Host GBP2 Loading. (
  • Gold DA Kaplan AD Lis A Bett GC Rosowski EE Cirelli KM Bougdour A Sidik SM Beck JR Lourido S Egea PF Bradley PJ Hakimi MA Rasmusson RL Saeij JP The Toxoplasma Dense Granule Proteins GRA17 and GRA23 Mediate the Movement of Small Molecules between the Host and the Parasitophorous Vacuole. (
  • Toxoplasma gondii is a widespread protozoan parasite that commonly infects domestic, wild, and companion animals ( 8 ). (
  • Toxoplasma is well adapted to mammalian hosts, being transmitted by ingestion of undercooked meat harboring tissue cysts and through food and water supplies contaminated with oocysts shed from cats ( 8 ). (
  • After helping to define extracellular survival tactics of African trypanosomes during graduate (Western University, with the infamous Barbara Burleigh) and postdoctoral studies (Rockefeller University), I became fascinated by the distinctive intracellular lifestyles of apicomplexan parasites including Toxoplasma gondii. (
  • Since then our work at Johns Hopkins University and the University of Michigan has helped define how Toxoplasma uses adhesive proteins to actively invade target cells and showed that its hybrid exo-endocytic system supports both protein secretion and ingestion of host derived material. (
  • We also identified the basis for Toxoplasma cytolytic egress from infected cells, defined the parasite's use of autophagy as a survival strategy during persistence, and we are developing inhibitors targeting a parasite lysosomal protease to interrupt chronic infection. (
  • Toxoplasma gondii is an obligate intracellular parasite infecting humans and other warm-blooded animals, resulting in serious public health problems and economic losses worldwide. (
  • Myristoylation of a secreted protein, identified in a global myristoylation analysis of the eukaryotic parasite Toxoplasma gondii , is important for host cell invasion. (
  • Toxoplasma Secretory Proteins and their Roles in Cell invasion and Intracellular Survival. (
  • A synthetic peptide derived from the parasite Toxoplasma gondii triggers human dendritic cells' migration. (
  • Recent studies on Plasmodium and Toxoplasma have demonstrated a role for parasite motility in the mammalian host and/or insect vector ( 19 - 21 , 52 , 58 , 70 ). (
  • Diagnostic tests for neosporosis are complicated by the potential for cross-reaction of antibodies to antigens that are similar between N. caninum and closely related parasites Toxoplasma gondii and Sarcocystis cruzi. (
  • We have a large, well-funded research team working on the temperate liver fluke parasite, Fasciola hepatica, the abortifacient protozoans Neospora caninum and Toxoplasma gondii , and the cyathostomins (the most significant group of gastro-intestinal nematodes affecting horses). (
  • Metallopeptidases from parasitic protozoa, including Toxoplasma , are investigated because of their crucial role in parasite biology. (
  • Les métallopeptidases provenant de protozoaires parasites, y compris Toxoplasma , sont étudiées en raison de leur rôle crucial dans la biologie du parasite. (
  • Toxoplasma gondii is an obligate intracellular apicomplexan protozoan parasite that is responsible for toxoplasmosis in humans and animals. (
  • To distinguish between these two basic mechanisms of cell-mediated immunity, reciprocal bone marrow chimeras were constructed between wild-type and IFN-γ receptor-deficient mice and their survival assessed following infection with Toxoplasma gondii , a protozoan parasite that invades both hemopoietic and nonhemopoietic cell lineages. (
  • Secretion of micronemal proteins is associated with Toxoplasma invasion of host cells. (
  • Soldati D, Dubremetz JF, Lebrun M. Microneme proteins: Structural and functional requirements to promote adhesion and invasion by the apicomplexan parasite Toxoplasma gondii. (
  • Pinniped- and Cetacean-Derived ETosis Contributes to Combating Emerging Apicomplexan Parasites ( Toxoplasma gondii , Neospora caninum ) Circulating in Marine Environments. (
  • We recently reported a new luciferase-based method for measuring microneme secretion in a 96-well format with high sensitivity in the model apicomplexan Toxoplasma gondii . (
  • Carruthers VB, Sibley LD (1999) Mobilization of intracellular calcium stimulates microneme discharge in Toxoplasma gondii . (
  • Carruthers VB, Moreno SNJ, Sibley LD (1999) Ethanol and acetaldehyde elevate intracellular [Ca 2+ ] calcium and stimulate microneme discharge in Toxoplasma gondii . (
  • Lovett JL, Marchesini N, Moreno SN, Sibley LD (2002) Toxoplasma gondii microneme secretion involves intracellular Ca 2+ release from IP 3 /ryanodine sensitive stores. (
  • Barragan A, Brossier F, Sibley LD (2005) Transepithelial migration of Toxoplasma gondii involves an interaction of intercellular adhesion molecule 1 (ICAM-1) with the parasite adhesin MIC2. (
  • Our research is focused on the formation of a structure (the moving junction ) which is essential for host cell invasion in both Toxoplasma and Plasmodium , and which depends on the cooperation between microneme and rhoptry proteins. (
  • Thiazolidinone derivatives show inhibitory activity (IC 50 ) against the Toxoplasma gondii parasite, as well as high selectivity with high therapeutic index. (
  • Toxoplasma gondii is a parasite that infects a large variety of mammals -including humans- and represents an important public health concern. (
  • Using state-of-the-art imaging techniques, we are also investigating how parasites, such as Toxoplasma gondii , can evade and manipulate host immune responses for their own benefit. (
  • Unlike the related pathogen used in infection models, Toxoplasma gondii , this is a natural, self-limiting, murine parasite, which induces a strong immune response and establishes long-lasting protection against subsequent infections. (
  • Merozoites of Plasmodium falciparum , the parasite responsible for the most dangerous form of malaria, invade erythrocytes using a family of adhesins called Duffy binding ligand-erythrocyte binding proteins (DBL-EBPs). (
  • Malaria is caused by species of Plasmodium , a protozoan parasite belonging to the phylum Apicomplexa. (
  • It should also be applicable during in vivo infections and in other apicomplexan parasites, including Plasmodium spp. (
  • The most familiar mechanism of biological transmission of blood parasites is by injection of the infectious agent when the insect bites, a method employed most notably by Plasmodium falciparum Welch, the causative agent of the deadliest form of human malaria. (
  • The thrombospondin-related anonymous protein (TRAP) was first discovered in the sporozoite of Plasmodium falciparum and TRAP family proteins are secreted by micronemes and transported to the parasite surface to participate in the invasion process. (
  • Zhang M et al (2010) Plasmodium sporozoite development in the mammalian host is controlled by phosphorylation of eukaryotic initiation factor 2? (
  • With malaria parasites ( Plasmodium spp. (
  • Apicomplexan parasites in the genera Babesia and Plasmodium invade and replicate within erythrocytes, resulting in, respectively, babesiosis and malaria ( 13 ). (
  • Erythrocytes infected with either Babesia bovis or Plasmodium falciparum are sequestered in the microvasculature as a result of parasite-induced adherence to endothelial cells ( 4 , 48 ). (
  • The cupredoxin family protein azurin, produced by Pseudomonas aeruginosa, exhibits a remarkable ability to impede invasion of a number of diverse intracellular pathogens, including the human AIDS virus human immunodeficiency virus type 1 and the protozoan parasite Plasmodium falciparum (which causes malaria). (
  • Thidiazuron inhibited growth of T. gondii and Plasmodium falciparum, a human malaria parasite, suggesting that thidiazuron has therapeutic potential as an inhibitor of apicomplexan parasites. (
  • Although T. gondii is primarily an opportunistic pathogen, it has emerged as a model for study of the biology of apicomplexan parasites, a group that contains Plasmodium spp. (
  • She is now studying the molecular and physiological interactions between the Anopheles vector and the Plasmodium malaria parasite both in the laboratory and in field settings. (
  • As a postdoc in Manoj Duraisingh's lab at Harvard School of Public Health she performed a genetic screen to identify critical host factors for Plasmodium falciparum malaria using red blood cells derived from hematopoietic stem cells. (
  • Her research is focused on understanding how host factors from the human erythrocyte influence the biology and pathogenesis of the malaria parasite Plasmodium falciparum. (
  • All the clinical symptoms of Plasmodium falciparum malaria are attributed to the blood stage of the parasite life cycle. (
  • Erythrocytes, which are incapable of endocytosis or phagocytosis, can be infected by the malaria parasite Plasmodium falciparum . (
  • Malaria infection is initiated when a mosquito injects Plasmodium sporozoites into a mammalian host. (
  • A striking feature of Plasmodium sporozoites, as well as invasive stages of other apicomplexan protozoa, is that they exhibit gliding motility, which results in translocation of the organism without any flexing or undulation of its body, nor participation of appendages such as cilia, flagellae or pseudopods. (
  • Red blood cell invasion by the malaria parasite Plasmodium falciparum relies on a complex protein network that uses low and high affinity receptor-ligand interactions. (
  • A lack of robust tools for genetic manipulation of the parasite limits functional analysis of these hypothetical proteins and other aspects of the Plasmodium genome. (
  • However, the lack of such advanced genetic approaches in Plasmodium is a major impediment to elucidating the parasite genome. (
  • The Medicines for Malaria Venture Malaria Box is a collection of over 400 compounds representing families of structures identified in phenotypic screens of pharmaceutical and academic libraries against the Plasmodium falciparum malaria parasite. (
  • During development in human erythrocytes, Plasmodium falciparum parasites display a remarkable number of adhesive proteins on their plasma membrane. (
  • A variety of protein complexes have previously been described for the human malaria parasite Plasmodium falciparum , like the actin-myosin motor complex enabling gliding motility of the invasive stages. (
  • The phylum Apicomplexa includes intracellular parasites causing immense global disease burden, the deadliest of them being the human malaria parasite Plasmodium falciparum , which invades and replicates within erythrocytes. (
  • Delayed death in the malaria parasite Plasmodium falciparum is caused by disruption of prenylation-dependent intracellular trafficking. (
  • Plasmodium falciparum has an obligate two host lifecycle, proliferative stages are only found in humans, sexual reproduction takes place in mosquitoes. (
  • In contrast , replication of apicomplexan parasites involves the internal budding of multiple daughter parasites inside a single mother (2 in case of T. gondii , circa 32 in case of blood stage Plasmodium spp . ). (
  • The most eminent of the apicomplexan parasites of humans are Plasmodium spp. (
  • The apicomplexan parasite Plasmodium falciparum causes the most severe form of malaria in humans. (
  • We have developed software for the prediction of exported proteins in the genus Plasmodium , and identified exported proteins conserved between malaria parasites infecting rodents and the two major causes of human malaria, P. falciparum and P. vivax . (
  • The presence of a conserved 'exportome' in the genus Plasmodium has important implications for our understanding of both common mechanisms and species-specific differences in host-parasite interactions, and may be crucial in developing novel antimalarial drugs to this infectious disease. (
  • Species of the genus Plasmodium are obligate intracellular parasites, switching between an arthropod vector and their respective vertebrate host, where they undergo cycles of asexual reproduction in erythrocytes. (
  • This sequence is functionally conserved across the genus Plasmodium , indicating the presence of a conserved export mechanism across the parasitophorous vacuole membrane in malaria parasites. (
  • The unique environment of the Fondation des Treilles was the setting for an interdisciplinary meeting focused upon interactions between Anopheline mosquitoes and Plasmodium parasites. (
  • In the absence of an effective vaccine against the Plasmodium parasite and with the emergence of drug-resistant parasite strains and insecticide-resistant mosquito vectors, it is realistic to predict a continuing worsening of this problem. (
  • The design and implementation of such an approach will require increased understanding of the complex interactions between insect and parasite during the mosquito stages of the Plasmodium life cycle. (
  • Robert E. Sinden's oral presentation was an overview of current knowledge and questions concerning the interactions that occur between vector and parasite during the development of Plasmodium in Anopheles. (
  • The Plasmodium parasite is adapted for growth and development within diverse physiological milieux, most strikingly the environments of the vertebrate host and insect vector. (
  • Dominic Kwiatkowski presented findings on the regulation of TNF synthesis during Plasmodium infection of humans as a consequence of 'malaria toxins' released during parasite growth. (
  • Apicomplexan pathogens are obligate intracellular parasites. (
  • Genome compaction in obligate intracellular pathogens such as microsporidia results in dependence on host resources to facilitate intracellular growth, and pathogen hijacking of host cell processes to redirect these resources. (
  • Beiting DP & Roos DS (2011) A systems biological view of intracellular pathogens. (
  • The complex interaction between intracellular (IC) pathogens and their eukaryotic host cells embodies the fundamental evolutionary struggle of eukaryotic cells to survive under a continuous challenge caused by the infecting pathogen. (
  • Movement of microbial pathogens plays an important role in pathogen biology, host-pathogen interaction, and disease pathogenesis. (
  • Microbial pathogens employ a variety of mechanisms for cell locomotion, including passive movement within their host's circulation, cooptation of host cytoskeletal and membrane transport pathways, and active self-propulsion through the action of flagellar, amoeboid, or gliding motility. (
  • Furthermore, some of these strategies may be used by pathogens to infect both tick and mammalian hosts. (
  • PLOS Pathogens publishes Open Access research and commentary that significantly advance the understanding of pathogens and how they interact with host organisms. (
  • Although interferon (IFN)-γ-activated, mononuclear phagocytes are considered to be the major effectors of resistance to intracellular pathogens, it is unclear how they control the growth of microorganisms that reside in nonhemopoietic cells. (
  • Nevertheless, the mechanisms by which the multicellular interactions involved in CMI lead to control of intracellular pathogens and protection of the invaded tissue have only been partially elucidated. (
  • Nonetheless, many intracellular pathogens infect not only cells of the mononuclear phagocyte lineage but also those of epithelial, endothelial, mesodermal, and neuronal derivation. (
  • Although the growth of such intracellular pathogens is generally thought to be controlled by toxic reactive nitrogen or reactive oxygen intermediates, it is unclear in many cases whether the latter effector molecules can be generated and/or function in the nonhemopoietic cell types that they invade. (
  • Thus such complexes are of importance for interactions between pathogens and between pathogens and their host cells. (
  • For intracellular pathogens, such as malaria parasites, recognition, adhesion and invasion of host cells are essential steps during infection and are often mediated by protein-protein interactions. (
  • Parasitic protozoans of the genus Theileria are intracellular pathogens that induce the cellular transformation of leukocytes, causing uncontrolled proliferation of the infected host cell. (
  • The Apicomplexa are obligate intracellular parasites and the phylum contains many well-known pathogens of humans and livestock. (
  • However, many of the pathogens used in mouse models are not natural to the host, can cause systemic inflammation or can persist in the tissues for long periods. (
  • Here we show that RON2 is inserted as an integral membrane protein in the host cell and, using several interaction assays with native or recombinant proteins, we define the region that binds AMA1. (
  • More importantly, invasion inhibition assays using recombinant proteins demonstrate that the RON2-AMA1 interaction is crucial for both T. gondii and P. falciparum entry into their host cells. (
  • Data analyses showed that host cells produce more proteins in response to infection with T. gondii than with N. caninum after 36 hours post infection (p.i. (
  • Knowledge pertaining to the host-parasite interaction could be bolstered by developing a system to specifically label parasite proteins while the parasite grows inside the host cell. (
  • The MetRS NLL -Anl system labels nascent T. gondii proteins in an orthogonal fashion, labeling proteins only in MetRS NLL -expressing parasites. (
  • Although this approach allows labeling of a diverse array of parasite proteins, secreted parasite proteins appear to be only minimally labeled in MetRS NLL -expressing T. gondii. (
  • The approach presented in this article provides the first method for specific labeling of T. gondii proteins while the parasite grows inside the host cell. (
  • We show that this approach is useful for pulse-chase labeling of parasite proteins during in vitro growth. (
  • in these species, the number of genes encoding exported proteins has increased significantly, suggesting that these genes might have emerged in the context of host-parasite interactions. (
  • Notably, both studies found that many apicomplexan genes previously linked to parasitism were also present in chromerids, and that chromerid genomes encode many proteins that contain functional domains implicated in molecular processes of apicomplexan parasites. (
  • More than 80 homologous genes annotated as being implicated in invasion showed statistically significant co-expression across different conditions in both species, suggesting that the genome of the proto-apicomplexan ancestor (the last common ancestor of chromerids and apicomplexans) encoded functionally linked proteins that have been utilized differently by free-living and parasitic lineages. (
  • Various TRAP proteins have been identified in apicomplexan protozoans, but there have been few reports about TRAP proteins in Babesia orientalis . (
  • The ability to saturate the T. gondii genome by insertional mutagenesis, target defined loci for genetic deletion or allelic replacement, and control the expression of recombinant proteins makes forward genetic approaches feasible in these parasites. (
  • Erythrocyte adhesion is mediated by parasite-encoded proteins, such as P. falciparum EMP-1, rosettin, and sequestrin ( 3 , 9 , 30 ), or, alternatively, by parasite modifications of host proteins ( 6 ). (
  • Importantly, both parasite-encoded proteins and modified host proteins may present new epitopes associated exclusively with infected cells and therefore may serve as targets of immunity as well as pathogenetic determinants ( 5 , 18 ). (
  • This complex formation is initiated by intermolecular interactions between the two secretory parasitic proteins-namely, apical membrane antigen 1 (AMA1) and rhoptry neck protein 2 (RON2) and is critically essential for the host invasion process. (
  • T-cell immunopeptidomes reveal cell subtype surface markers derived from intracellular proteins. (
  • Because invasion is considered a requirement for pathogen survival and replication within the host, the identification of secreted proteins (secretome) involved in invasion may be useful to reveal interesting targets for therapeutic intervention. (
  • An interaction network was built by computational prediction involving the up- and down-regulated proteins. (
  • Information from the network interaction and up-regulated proteins was important to recognise key proteins potentially involved in the metabolic regulation of secretion. (
  • As with all apicomplexan species, N. caninum is an obligate intracellular parasite that invades the host cell in a conserved active manner, which involves the release of proteins from phylum-specific secretory organelles and the activation of the parasite invasion motor. (
  • AMA1 Proteins secreted onto the parasite surface from apical organelles, the micronemes, are thought to play an important role in invasion. (
  • Proteins of the parasite's motility apparatus, including the myosin motor protein, MyoA, are highly conserved across apicomplexan parasites but absent or divergent in higher eukaryotes, suggesting that they may be useful drug targets. (
  • Using tachypleginA and other motility-inhibiting compounds as chemical probes, together with parasites containing mutations in proteins of the motility apparatus and a variety of assays we have developed to study motor function, we are attempting to develop a detailed mechanistic understanding of how T. gondii and related parasites move over, around and into cells of their hosts during infection. (
  • Analysis of MIC8 has demonstrated that it is, like other micronemal transmembrane proteins, secreted upon an increase in intracellular calcium concentration and processed close to its transmembrane domain (TMD). (
  • Als proteins are thought to act as adhesin molecules binding to host tissues. (
  • Many of the key parasite proteins that bind host receptors are localized in apical organelles called micronemes. (
  • We find that a transmembrane protein (Duffy), glycosylphosphatidylinositol (GPI)‐anchored and cytoplasmic proteins, associated with detergent‐resistant membranes (DRMs) that are characteristic of microdomains in host cell membranes, are internalized by vacuolar parasites, while the major integral membrane and cytoskeletal proteins are not. (
  • The internalized host proteins and a plasmodial transmembrane resident parasitophorous vacuolar membrane (PVM) protein are detected in DRMs associated with vacuolar parasites. (
  • Furthermore, novel mechanisms regulated by the DRM lipids, sphingomyelin and cholesterol, mediate (i) the uptake of host DRM proteins and (ii) maintenance of the intracellular vacuole in the non‐endocytic red cell, which may have implications for intracellular parasitism and pathogenesis. (
  • Using pharmacological activators and inhibitors, we have concluded that gliding motility is initiated when albumin interacts with the surface of the sporozoite and that this leads to a signal transduction cascade within the sporozoite, including the elevation of intracellular cAMP, the modulation of sporozoite motility by Ca 2+ and the release of microneme proteins. (
  • Studies with apicomplexans have used several different approaches to provide evidence of microneme secretion, including quantification of microneme proteins secreted into the medium, immunofluorescence studies to detect microneme proteins expressed on the parasite surface, fine structural analysis of microneme contents and their appearance on the parasite surface after microneme discharge, and gliding motility. (
  • This process is driven by the intracellular translocation machinery of the parasite involving transmembrane proteins connected to the actinomyosin contractile system [ 7 ]. (
  • Upon secretion from these organelles, some of these proteins function as cellular adhesins that mediate host-cell penetration and subsequent establishment within the red blood cell [ 9 ]. (
  • In gametocytes, sexual precursor cells mediating parasite transmission to the mosquito vector, plasma membrane-associated proteins primarily belong to the Pf CCp and 6-cys families with roles in fertilization. (
  • Microneme proteins secreted in the early stages of this process participate in attachment to the host cell and subsequent formation of the connection with the parasite actinomyosin system, thereby providing the platform from which to drive invasion [3] . (
  • Central to these processes is the timely engagement and disengagement of specific receptors upon the regulated release of apical invasion proteins from parasite secretory organelles (micronemes, rhoptries). (
  • In this short review, we summarise recent progress on identification and functional characterisation of apical invasion proteins mobilised to the parasite surface from the microneme organelles. (
  • Mix and match modules: Structure and function of microneme proteins in apicomplexan parasites. (
  • Indirect immunofluorescence analysis with a pan-nuclear pore complex antibody, combined with overexpression of a panel of nuclear pore proteins, revealed that the parasite recruits nuclear pore complex components close to its surface. (
  • Little is known about how the parasite communicates with its host or by what route secreted parasite proteins are translocated into the host, and we propose that nuclear trafficking machinery at the parasite surface might play a role in this. (
  • Microneme vesicles hold adhesins and other proteins that are secreted to facilitate parasite attachment, invasion of host cells, and egress following replication-all processes indispensable for cell-to-cell transmission of these obligate intracellular parasites. (
  • However, the classical method of measuring microneme secretion by immunoblotting for microneme proteins in parasite excreted/secreted antigen (ESA) preparations is low-throughput and only semiquantitative. (
  • Microneme proteins contribute to motility, attachment and invasion, while rhoptry proteins contribute to both invasion and subsequent manipulation of host cell functions after the parasites have established themselves in their host cells. (
  • The complex of RON2, RON4, RON5 and RON8 localize to the host cytosol and cooperate to recruit adaptor proteins (ALIX, CD2AP, CIN85, TSG101) through multiple specific interaction motifs that physically link the RONs complex to the cortical actin cytoskeleton. (
  • They inject parasite proteins directly in the cytoplasm of host cells not only for invasion but also to hijack host functions crucial to establish and maintain infection. (
  • To disclose the target proteins of the thiazolidinone core in this parasite, we explored in silico the active sites of different T. gondii proteins and estimated the binding-free energy of reported thiazolidinone molecules with inhibitory effect on invasion and replication of the parasite inside host cells. (
  • The best binding affinity was observed in the active site of kinase proteins, we selected the active site of the T. gondii ROP18 kinase, because it is an important factor for the virulence and survival of the parasite. (
  • After invasion into erythrocytes, asexual parasite stages drastically alter their host cell and export remodeling and virulence proteins. (
  • Previously, we have reported identification and functional analysis of a short motif necessary for export of proteins out of the parasite and into the red blood cell. (
  • Once inside the infected erythrocyte the parasite resides in a parasitophorous vacuole, which acts as a biochemical barrier between parasite and host through which parasite proteins must be translocated to reach the parasite-infected erythrocyte cytosol and the host cell membrane. (
  • The PEXEL sequence has allowed the prediction of proteins exported into the host erythrocyte, which are likely to be important to both erythrocyte remodeling and virulence. (
  • Due to the importance of protein-protein interactions (PPIs) and multiple protein complexes (MPCs) in host-parasite interactions, blue native polyacrylamide gel electrophoresis (BN-PAGE) combined with liquid chromatography tandem mass spectrometry (LC MS/MS) was used to study T. gondii and N. caninum tachyzoites. (
  • In addition, in T. gondii the microneme MIC1/6 complex was found migrated and/or co-associated with the important surface antigen glycoprotein SAG1, which is critical in the initial interaction with host surface peptidoglycan. (
  • phosphopeptide enrichment, combined with LC MS/MS has been used to study the global response in the host signalling pathway through protein phosphorylation and signal transduction in response to infection with T. gondii and N. caninum. (
  • about one-third of the phosphoproteomes of the host cell in response to infection by T. gondii and N. caninum was different. (
  • Approximately 21 % of the phospho-motifs were found differentially enriched between host cells infected with T. gondii compared to N. caninum infection and finally the pathway analysis showed that a few pathways were differentially enriched between infections with these parasites, such as glycolysis/gluconeogenesis and mTOR signalling pathway in infection with T. gondii Abstract vi but not with N. caninum. (
  • How T. gondii is able to modulate the host cell to support itself is still poorly understood. (
  • IMPORTANCE Studying how T. gondii modifies the host cell to permit its survival is complicated by the complex protein environment of the host cell. (
  • T. gondii has the ability to infect all tissue types in the affected host, however, this parasite has preference for the brain and muscles, where it remains for a long time in these tissues as dormant cysts. (
  • Intriguingly, in T. gondii , ATG8 localizes to the apicoplast under normal intracellular growth conditions. (
  • T. gondii invades the host cell by forming a moving junction (MJ) complex. (
  • Toxoplasmosis is caused by a one-celled protozoan parasite known as T. gondii. (
  • In the present study we demonstrate that upon oral infection with T. gondii cysts, chronically infected BALB/c mice lost over time their natural fear against cat urine which was paralleled by the persistence of the parasite in brain regions affecting behaviour and odor perception. (
  • T. gondii can only multiply within cells of its host, and repeated cycles of host cell invasion, parasite multiplication and host cell lysis are a major cause of the tissue damage that occurs during acute infection. (
  • A better understanding of the mechanisms of host cell invasion by T. gondii is therefore important to the development of new approaches to treating toxoplasmosis. (
  • T. gondii is also a powerful model for studying the invasion of related apicomplexan parasites, including those that cause malaria and cryptosporidiosis. (
  • We are currently studying two aspects of T. gondii AMA1 critical to its role in mediating invasion: (a) the function of its cytosolic tail and (b) why and how its extracellular domain is cleaved and shed from the parasite surface during invasion. (
  • In addition to providing new insights into the mechanisms of host cell invasion, this work has clear drug development implications for T. gondii and other apicomplexan parasites. (
  • Like related tissue coccidians, T. gondii has a complex life cycle alternating between a sexual cycle, which occurs only within enterocytes of the small intestines of cats (all members of the Felidae appear to be susceptible), and asexual propagation in a variety of warm-blooded vertebrate hosts ( 8 ). (
  • Humans are accidental hosts of T. gondii , yet seroprevalence rates indicate high rates of chronic infection in many countries of Europe and Central and South America ( 16 ). (
  • Rhoptries are involved in T. gondii invasion and host cell interaction and have been implicated as important virulence factors. (
  • Here, we show that the micronemal protein MIC8 of T. gondii is essential for the parasite to invade the host cell. (
  • A genetic screen in combination with biochemical approaches reveal hijacking of the host β-catenin destruction complex by the parasite T. gondii to reprogram immune gene expression. (
  • Dans la présente étude, nous avons examiné la base de données de T. gondii en utilisant des motifs PFAM spécifiques des métallopeptidases en association avec la base de données de peptidases MEROPS (version 10.0). (
  • In the cis model, the lymphokines directly activate the somatic cell to suppress intracellular T . gondii growth. (
  • T. gondii can infect multiple hosts and different tissues and cell types. (
  • 4 ] experimentally proved T. gondii as deficient in cholesterol biosynthesis and showed that this parasite scavenges cholesterol from its host cell. (
  • However, different strategies were described in different T. gondii -infected host cell types. (
  • Schematic of T. gondii tachyzoite invading a host cell. (
  • T. gondii belongs to the phylum Apicomplexan and is distributed globally. (
  • Furthermore, the parasite can develop resistance to this treatment and its susceptibility to PYR varies among T. gondii strains. (
  • Obligate intracellular Apicomplexa parasites share a unique invasion mechanism involving a tight interaction between the host cell and the parasite surfaces called the moving junction (MJ). (
  • This work provides the first evidence that AMA1 uses the rhoptry neck protein RON2 as a receptor to promote invasion by Apicomplexa parasites. (
  • The malaria parasite is the most important member of the Apicomplexa, a large and highly successful phylum of intracellular parasites. (
  • All Apicomplexa adopt a common mode of host-cell entry, but individual species incorporate unique features and utilize a specific set of ligand-receptor interactions. (
  • While some Apicomplexa can invade many different host cells, the disease-associated blood-stage form of the malaria parasite is restricted to erythrocytes. (
  • The phylum Apicomplexa contains some of the most widespread protozoan parasites of humans and animals. (
  • The protozoan phylum Apicomplexa is extremely species rich and members of this group are found as parasites in virtually every vertebrate and many invertebrate animals. (
  • This model system will enable us to advance the fundamental knowledge on the evolutionary steps of symbiosis in the Apicomplexa, identifying key cellular and molecular transitions in the evolution from free-living relatives to intracellular parasites. (
  • Apicomplexa contains a large assortment of single celled eukaryotic organisms, known to parasitise vertebrates (including humans) and invertebrate hosts. (
  • The use of electron microscopes has led to the discovery of unique intracellular structures that led to the description of Apicomplexa as well as their sub-grouping (Levine, 1973). (
  • Microsporidia comprise a phylum of fungal-like obligate intracellular parasites that infect all phyla of animals, including humans and agriculturally important animals ( Vavra and Lukes 2013 ). (
  • The increase in parasite cytosolic Ca 2+ upon contact with the host cell mediates critical events, including the exocytosis of phylum-specific secretory organelles and the activation of the parasite invasion motor. (
  • Although the zoite form is a structurally conserved start and end point of each cycle, the course of intracellular development has considerable morphological and functional diversity across the phylum. (
  • can be an intracellular zoonotic parasite that chronically infects 30% from the world's population [1]. (
  • can be an obligate intracellular apicomplexan parasite that infects warm-blooded vertebrates, including human beings. (
  • This device outlines the protocols for and development and maintenance of is normally a ubiquitous, one cell protozoan parasite that infects any nucleated cell in wild birds and vertebrates world-wide. (
  • Eimeria vermiformis is a tissue specific, intracellular protozoan that infects the murine small intestinal epithelia, which has been widely used as a coccidian model to study mucosal immunology. (
  • Eimeria vermiformis is a tissue specific, intracellular single cell protozoan, which infects the small intestinal epithelia. (
  • 2019 Jun 24;60:117-123 Authors: Escoll P, Buchrieser C Abstract The limited metabolic resources of a cell represent an intriguing 'conflict of interest' during host-pathogen interactions, as the battle for nutrients might determine the outcome of an infection. (
  • In turn, infection by intracellular bacteria provokes metabolic alterations of the host cell that benefit the pathogen. (
  • The study of the host-driven and pathogen-driven metabolic alterations that seem to co-exist during infection is an emerging field that will define the metabolic pathways that might be targeted to combat infection. (
  • Here, we perform a genetic screen to identify host transcription factors important for development of the microsporidian pathogen Nematocida parisii inside intestinal cells of its natural host, the nematode Caenorhabditis elegans . (
  • Studies in the Roos laboratory employ modern cell biological, molecular genetic, biochemical/pharmacological, immunological and genomic/bioinformatic techniques to study protozoan parasites, eukaryotic evolution, and the biology of host-pathogen interactions. (
  • For most of the parasites discussed here the ability to penetrate biological barriers and/or to establish intracellular residence is critical to survival of the pathogen in the mammalian hosts. (
  • These observations indicate that Laz can serve as an important tool in the study of host-pathogen interactions and is worthy of further study for development into potential therapeutic agents. (
  • As an obligate IC pathogen, N. caninum survival is dependent upon entry, growth and development within the eukaryotic host cell and then exiting to initiate a new infection cycle. (
  • Her work on Trypanosoma cruzi, the protozoan parasite that causes human Chagas disease, addresses fundamental questions regarding the mechanistic basis of host cell colonization by this obligate intracellular pathogen with a focus on the permissive roles of host cell signaling and metabolism in this process. (
  • Host-Pathogen interaction: At the frontier of cellular microbiology . (
  • the contribution of cell motility to host-pathogen interactions has been largely unexplored. (
  • These determinants affect traits such as tick-host-pathogen and susceptibility to pathogen infection. (
  • Therefore, the elucidation of the mechanisms involved in tick-pathogen interactions that affect vector competence is essential for the identification of molecular drivers for tick-borne diseases. (
  • In this review, we provide a comprehensive overview of tick-pathogen molecular interactions for bacteria, viruses, and protozoa affecting human and animal health. (
  • Identification of interactions that promote tick survival, spread, and pathogen transmission provides the opportunity to disrupt these interactions and lead to a reduction in tick burden and the prevalence of tick-borne diseases. (
  • Current work in Paul's laboratory is focused on furthering the understanding of the role of lipid biosynthesis and membrane trafficking in host-pathogen interactions, with a view to elucidating protozoan specific activities amenable to therapeutic intervention. (
  • system to review host-pathogen interactions. (
  • We use advanced 3D tissue culture models to study host-pathogen interactions at the intestinal epithelium, with particular emphasis on apicomplexan parasites. (
  • knowledge that will increase our appreciation of host-pathogen interactions, while facilitating vaccine design. (
  • The information obtained from using this mouse model can reveal fundamental mechanisms of interaction between the pathogen and the immune response, e.g. , provided by intraepithelial lymphocytes (IEL) at the basolateral site of epithelial cells but also a variety of other immune cell populations present in the gut. (
  • It is therefore an ideal pathogen to study the mechanisms of host protection against primary and secondary infection at the small intestinal barrier. (
  • Here, we discuss the state-of-the-art knowledge on metabolic reprogramming of host cells upon activation or infection with intracellular bacteria. (
  • As a means of understanding the broader host response to infection with these parasites at the systems biology level, integrated data analyses were performed on quantitative data from the transcriptome, proteome and phosphoproteome of host cells infected with the two parasites. (
  • Both infection routes result in the infection of intestinal cells after which the parasites develop into tachyzoites, which are the fast-growing, disseminating form of the parasite. (
  • These tools have been exploited to elucidate such diverse phenomena as the molecular mechanisms of drug action and resistance, temporal and developmental controls regulating differentiation through the complex parasite life cycle, host responses to infection, and the population biology of parasite evolution. (
  • To understand the sequential interactions between B. besnoiti and the host cell, transmission electron microscopic examinations were carried out on infected Vero cells fixed at various time intervals following infection with Besnoitia merozoites. (
  • Although Nephromyces was first described as a parasite, its ubiquity in molgulids argues strongly for Nephromyces infection as a net benefit to its molgulid hosts. (
  • The results show that infection of broilers with Eimeria and different C. perfringens strains, independent of their pathogenicity, decreases the expression of a 40-45 kDa host collagenase in the jejunum, as compared to the expression in Eimeria-infected control birds. (
  • These results indicate that host collagenases are not elicited by the C. perfringens infection for permeabilizing the host mucosa to allow penetration of the NetB toxin in Eimeria infected broilers. (
  • The changing pattern of extracellular metabolites suggests that HBMECs are target of metabolic alterations in N. caninum infection, which seem to reflect the changing metabolic state of infected cells and constitute a level of information exchange that host and parasite use to coordinate activities. (
  • The IC infection cycle ends up with lysis of the host cell and release of the parasite progeny. (
  • Despite significant research efforts understanding of the cellular processes by which N. caninum initiates infection and cause disease remains incomplete, partly, due to the complexity of N. caninum-host interaction, which determines the host response and outcome of infection. (
  • For example, our knowledge about the substrates used by N. caninum during infection, and the effect of N. caninum infection on the metabolism of the host cell is unknown. (
  • Giving the significant animal health implication and economic losses associated with N. caninum infection better understanding of the biochemical and metabolic changes in BBB cells induced by N. caninum and the metabolic requirement of N. caninum during infection is essential in order to understand the parasite neuro-pathogenesis. (
  • Motility Parasite motility is important for parasite movement into and out of host cells, for crossing biological barriers and for dissemination through the body during infection. (
  • Her laboratory studies the earliest stages of the malaria infection: The inoculation of sporozoites by infected mosquitoes and the significant physical and immunological obstacles that must be overcome for the parasite to establish infection in the mammalian host. (
  • Some intracellular parasites have also mastered the art of persistence for transmission or reemergence later in infection. (
  • Host-parasite interactions were investigated by RNA-Seq at two post-infection (pi) time points: 12 hpi, when tachyzoites have already invaded host cells, and 32 hpi, when tachyzoites have replicated for at least two generations. (
  • Finally, the influence of bovine viral diarrhea virus (BVDV) co-infection on the host cell machinery, and consequently on B. besnoiti invasion and proliferation, was investigated in BAECs. (
  • This review summarises and discusses current information available and gaps in research on malaria co-infection with gastro-intestinal helminths and tissue-dwelling parasites with emphasis on helminthic infections, in terms of the effects of migrating larval stages and intra and extracellular localisations of protozoan parasites and helminths in organs, tissues, and vascular and lymphatic circulations. (
  • Efforts in drug discovery and vaccine development are hindered by limited knowledge of the underlying cellular and molecular mechanisms of host-parasite interactions during co-infection and polyparasitism [ 10 , 11 ]. (
  • In the past three decades, several studies have been undertaken to establish the nature of interaction that occurs between soil-transmitted helminths (STHs) and malaria during co-infection scenarios. (
  • During transmission of Trypanosoma cruzi , lysophosphatidylcholine (LPC, " Lysophosphatidylcholine: a novel modulator of Trypanosoma cruzi transmission ") is introduced with vector's secretions and recruits host cells, promoting infection. (
  • Similarly, Leishmania amazonensis parasites express phosphatidylserine (PS, " Subversion of immunity by Leishmania amazonensis parasites: possible role of phosphatidylserine as a main regulator "), mimicking apoptotic cells to inhibit host cell activation and exacerbate infection. (
  • Together, these findings suggest that, in concert with bone marrow-derived effectors, nonhemopoietic cells can directly mediate, in the absence of endogenous iNOS, IFN-γ- and TNF-α-dependent host resistance to intracellular infection. (
  • Infection by apicomplexans is established in the host by rapid and forced invasion of host cells using a multistep process [2] . (
  • We here analyzed the influence of E. bovis infection on endothelial host cell cholesterol metabolism and found considerable differences to other coccidian parasites. (
  • Besnoitia besnoiti infection alters both endogenous cholesterol de novo synthesis and exogenous LDL uptake in host endothelial cells. (
  • Catherine Suarez won the best poster award at the EMBO workshop Molecular Advances and Parasite Strategies in Host Infection in Les Embiez (30 sept - 3 oct). (
  • Women who acquire the infection during pregnancy transmit the parasite to the fetus by congenital infection, affecting its development, which can be lethal in immunocompromised individuals. (
  • This mouse infection model is valuable to investigate the mechanisms of host protection against primary and secondary infection in the small intestine. (
  • A single sporulated oocyst can initiate an infection when swallowed by its respective host, the mouse. (
  • Thus, microsporidia undergo all of their replication inside of the host cell. (
  • These include one form of passive transmission in which the parasite is carried by the insect host without engaging in multiplication, and two forms of biological transmission in which the parasite undergoes development or replication in the insect host. (
  • Depletion of TgATG8 led to rapid loss of the organelle and subsequent intracellular replication defects, indicating that the protein is essential for maintaining apicoplast homeostasis and thus for survival of the tachyzoite stage. (
  • TgATG8 is crucial for normal replication of the parasite inside its host cell. (
  • Inside the erythrocytes, the merozoite differentiates into a trophozoite, which undergoes asexual replication to produce daughter merozoites able to exit the host cell and invade additional erythrocytes ( 13 ). (
  • As described elsewhere, interactions between apoptotic cells and T. cruzi -infected macrophages induce intracellular parasite replication [ 4 ]. (
  • Consequently, LDL supplementation significantly improved parasite replication. (
  • Overall, these results show that E. bovis considerably exploits the host cell cholesterol metabolism to guarantee its massive intracellular growth and replication. (
  • The objectives of our team are to decipher cellular and molecular features related to two essential parasitic functions: host cell invasion and intracellular replication, with the aim of identifying novel therapeutic strategies. (
  • While most eukaryotic cells replicate by binary fission , replication of apicomplexan parasites involves the assembly of daughters ( merozoites /tachyzoites) within the mother cell, using the so- called Inner Membrane Complex ( IMC ) as a scaffold . (
  • Although the temporal organization of morphological changes of organelles during replication of apicomplexan parasites has been well documented by several groups [4] , [5] to date almost nothing is known about the molecular mechanisms involved . (
  • During replication a scaffold for the assembly of daughter parasites is built that is known as the Inner Membrane Complex (IMC). (
  • As daughter parasites grow they acquire a complete set of organelles, via de novo synthesis (i.e. micronemes and rhoptries), or replication/segregation (i.e. (
  • It is important to investigate the involvement of mosquitoes, frogs and parasites in this interaction in order to understand the consequences of anthropogenic actions, such as implementing biocontrol efforts against mosquitoes, and to determine potential causes of the global decline of amphibian species. (
  • Lesser known are species that preferentially feed on ectothermic hosts such as frogs and snakes. (
  • The authors noted that the proto-apicomplexan ancestor possessed all known flagellar components - which are essential for motility of the free-living species - whereas these components were progressively lost as individual apicomplexan lineages differentiated, possibly owing to their adaptation to a parasitic lifestyle. (
  • even though prevalence in parasitic associations can also sometimes be locally high in particular host populations or environmental conditions, overall prevalence of a parasite within a given host species nevertheless varies over space and time. (
  • Each insect can be the host of multiple species. (
  • In all species, four or more sporozoites (the precise number depends on the species) equipped with an apical complex escape from the oocysts, a process called excystation, find their way to the appropriate body cavity, and penetrate host cells in their immediate environment. (
  • Most species have monoxenous lifecycles involving a single invertebrate host. (
  • Merogony may be intracellular or extracellular depending on the species. (
  • is the largest and most diverse genus of apicomplexan parasites and some species of the genus are the causative agent of coccidiosis, a disease economically devastating in poultry. (
  • Trypanosoma brucei species are kinetoplastid parasites that infect a large variety of mammals, causing severe disease in domestic animals with important economic losses in endemic countries. (
  • This approach will be assessed by infecting the host cells with the target species and monitor the success of gregarine development and propagation using an in-house automated microscopy system, under controlled atmospheric conditions. (
  • It is estimated that out of a probable 1.2 - 10 million apicomplexan species, only about 0.1% have been named and described to date (Adl et al. (
  • 2011). How parasite burden and pathology in captive animals translate into the wild is of much interest, especially when large resources are being placed into captive breeding programs of endangered species. (
  • Furthermore, E. vermiformis is monoxenous, its life cycle is completed without the need of a second host species (see Figure 1). (
  • This article presents the ultrastructural dynamics of host cell invasion and intracellular survival of Besnoitia besnoiti. (
  • In biological terms, a parasite can be defined as an organism that grows, feeds and is sheltered on, or in, a different organism while contributing nothing to the survival of the host.1 This relationship is particularly intimate for parasitic protozoa (and single-celled fungi such as the Microsporidia), many of which not only penetrate tissue barriers, but gain entry into host cells. (
  • The common feature of IgM binding to the parasitized erythrocyte surface among otherwise genetically and antigenically distinct B. bigemina strains is suggestive of an advantageous role in parasite survival in vivo. (
  • The survival of the intracellular protozoan parasite Neospora caninum depends on its ability to adapt to changing metabolic conditions of the host cell. (
  • it functions in chemotaxis, survival in the environment, host cell attachment and invasion, intracellular locomotion, colonization of host tissues, and dissemination within the host ( 46 , 49 , 53 ). (
  • Parasites depend on their host for survival, since the host provides nutrition and protection. (
  • As a result of this dependence, parasites have considerable modifications to optimise parasitic nutrition and therefore their survival. (
  • In humans and other intermediate hosts, infections are the result of digesting parasites shed in felid feces or present in undercooked meat [ 4 ]. (
  • T. brucei and related subspecies, are uniflagellated parasites that cause African trypanosomiasis in humans and in wild and domestic animals. (
  • This special issue includes original papers and reviews that summarize current advances in our understanding on the mechanisms of immunity to protozoan parasites in humans and experimental animal models. (
  • We use the latest functional genomic and proteomic techniques to understand the basic biology of parasites that cause endemic intestinal diseases in humans, such as cryptosporidiosis, giardiasis and amoebiasis, in the UK and worldwide. (
  • While a large portion of the apicomplexans are known parasites of virtually all vetrebrates including humans, they are equally diverse in both marine and terrestrial invertebrates. (
  • Since in vivo and in vitro models of toxoplasmosis exist, and genetic manipulation has become possible, this protozoan parasite has recently been accepted as a model for understanding the pathogenesis and persistance of other intracellular parasites. (
  • Parasite motility is therefore essential for virulence and pathogenesis. (
  • parasite differentiation is required to elucidate the pathogenesis of the disease as well as for the introduction of fresh therapeutic methods to get rid of latency. (
  • An important question in malaria pathogenesis concerns the initial invasion of hepatocytes by the sporozoite stage parasites that are introduced during mosquito blood feeding. (
  • She is interested in exploring various facets of disease vectors focusing on sand flies that transmit Leishmania parasites by bite. (
  • Four papers of this special issue discuss molecules present at initial encounter between hosts and protozoan parasites plus the secretions of their insect vectors. (
  • Besnoitia besnoiti is an obligate intracellular coccidian protozoa of significant economic importance in the regions where it occurs. (
  • For most protozoa, however, a specific requirement for active parasite movement remains strongly implied but not tested. (
  • Many protozoa cause infections that often follow chronic courses, owing to coevolution between parasites and host immune system. (
  • Various studies have attempted to characterise these transporters in a number of parasites e.g. the amino acid transporter molecules in protozoa. (
  • These structural defects are linked to a diminished ability of the parasite to move and to invade host cells, as well as decreased secretion of effectors important for these processes. (
  • As an obligatory intracellular parasite, N. caninum needs to invade the host cell in an active manner to survive. (
  • Apicomplexan parasites actively invade the host cell in a complex, organised, stepwise process ( Carruthers and Boothroyd, 2006 ) that involves specialised secretory organelles (the micronemes, rhoptries and dense granules) and a unique form of movement termed gliding motility ( Soldati and Meissner, 2004 ). (
  • During the blood stage, malaria parasites invade and multiply within host erythrocytes. (
  • The intra-erythrocytic stage of the life cycle is initiated when liberated P. falciparum merozoites invade and multiply within host red blood cells. (
  • The clinical manifestations of malaria are caused by the asexually reproducing haploid blood stages, which invade erythrocytes and establish themselves within a parasitophorous vacuole (PV) within the host cell. (
  • The invasive stages (zoites) of most apicomplexan parasites are polarised cells that use their actinomyosin-powered gliding motility or "glideosome" system to move over surfaces, migrate through biological barriers and invade and leave host cells. (
  • These are released off their cysts and invade enterocytes of the tiny intestine changing into schizonts [4 5 The parasite inhabitants that develops in kitty enterocytes undergoes a traditional coccidian cycle regarding many rounds of asexual department and amplification accompanied by differentiation into macro- and microgamonts the dimorphic levels of sexual advancement. (
  • After de novo synthesis of the IMC and biogenesis or segregation of new organelles , daughters bud out of the mother cell to invade new host cells. (
  • The vacuole is later dissolved by babesial but not plasmodial parasites ( 11 , 37 ). (
  • Derived from host plasma membrane, the vacuole is rendered nonfusogenic with the host endolysosomal system. (
  • Invasion is coupled to the rhoptry-mediated formation of the parasitophorous vacuole in which the parasite resides in the cytoplasm of its host. (
  • The Bradley lab is focusing on the role of the rhoptries in the invasion of host cells, creation of the parasitophorous vacuole in which the parasite resides, and host-parasite interaction. (
  • AMA1, a protein secreted from micronemes and associated with the parasite surface during invasion, has been shown in vitro to bind the MJ complex through a direct association with RON2. (
  • for example, the striated fibre assemblin (SFA) protein has been conserved in all apicomplexan genomes. (
  • The movement complex is formed when a transmembrane protein is attached to a receptor located in the surface of the host cell. (
  • However, p94 was not encoded by B. bigemina and was not a parasite-modified erythrocyte membrane protein. (
  • We use mass spectrometry-based approaches which can do more than simply determining the identity of a protein isolated in a polyacrylamide gel -- rapidly advancing technologies are allowing us to measure dynamic changes in protein abundances, post-translational modification states, splice isoforms, interaction partners, and localization across multiple cell states. (
  • Our lab focuses on developing new methods in protein fractionation, instrumentation, and data analysis to meet these challenges, and then applies them to studying important biomedical paradigms, including antigen presentation in cancer, and monitoring host responses to the gut microbiome. (
  • Here, myectomy tissue from patients with obstructive hypertrophic cardiomyopathy and heart failure is analyzed using RNA-Seq, and the results are used to develop individualized protein-protein interaction networks. (
  • From this approach, hypertrophic cardiomyopathy is distinguished from dilated cardiomyopathy based on the protein-protein interaction network pattern. (
  • These proof-of-concept findings introduce personalized protein-protein interaction networks (reticulotypes) for characterizing patient-specific pathobiology, thereby offering a direct strategy for advancing precision medicine. (
  • We have also produced a panel of monoclonal antibodies against the rhoptry fraction, one of which has been used to identify a rhoptry-localized protein that is targeted to the host cell nucleus, establishing a new role for the rhoptries in host-parasite interaction. (
  • We furthermore demonstrate that the cytosolic domain is crucial for the function of MIC8 and can not be functionally complemented by any other micronemal protein characterised so far, suggesting that MIC8 represents a novel, functionally distinct invasion factor in this apicomplexan parasite. (
  • In the poster section, Joanna Shisler (University of Illinois at Urbana-Champaign [UIUC], Urbana) reported that the modified virus, Ankara, activates nuclear factor κB through the mitogen-activated protein kinase, extracellular signal-regulated kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway, possibly facilitating the host immune response. (
  • To provide a sensitive and specific assay for detecting antibodies to N. caninum in the serum of infected animals, we have investigated a recombinant form of the antigen known as Ncp29 (rNcp29), which is a major surface protein of the parasite. (
  • Invasion of erythrocytes by P. falciparum merozoites is a complex multi-step process that is mediated by specific molecular interactions between red cell surface receptors and parasite protein ligands [1] , [2] . (
  • Rather, as shown for Duffy, intracellular accumulation occurs at the same rate as that seen for a DRM‐associated GPI‐anchored protein. (
  • Since WD40 domains are known to mediate protein-protein contact by serving as a rigid scaffold for protein interactions, the presented data suggest that Pf WLP1 supports the stability of adhesion protein complexes of the plasmodial blood stages. (
  • We show that the major MARR protein from Eimeria tenella , EtMIC3, is deployed at the parasite-host interface during the early stages of invasion. (
  • The cytoskeletal protein actin is well conserved within apicomplexans but divergent from mammalian actins, and was primarily reported to function during host cell invasion. (
  • Defining the protein repertoire of microneme secretory organelles in the apicomplexan parasite Eimeria tenella. (
  • In the poster section, Joanna Shisler (University of Illinois at Urbana-Champaign [UIUC], Urbana) reported that the modified virus, Ankara, activates nuclear factor κB through the mitogen-activated protein kinase, extracellular signal–regulated kinase (MEK)/extracellular signal–regulated kinase (ERK) pathway, possibly facilitating the host immune response. (
  • It is believed that the WD40 repeats mediate protein-protein interactions andmembers of the family are involved in signal transduction, RNA processing, gene regulation,vesicular trafficking, cytoskeletal assembly and may play a role in the control of cytotypicdifferentiation. (
  • Importantly , Rab11A can be found in association with Myosin - Tail - Interacting - Protein (MTIP), also known as Myosin Light Chain 1 ( MLC1 ), a member of a 4-protein motor complex called the glideosome that is known to be crucial for parasite invasion of host cells. (
  • To fully understand these biological differences, the host-parasite interactions of these parasites have been investigated in this study using several different approaches at the molecular level. (
  • The molecular machinery of autophagy was identified mainly in model organisms such as yeasts but remains poorly characterized in phylogenetically distant apicomplexan parasites. (
  • In the ensuing 18 chapters, select members of this diverse set of protozoan parasites, as well as some examples of the extremely reduced fungal parasites classified as Microsporidia, are discussed within the context of the fascinating molecular strategies employed by these organisms to migrate across biological barriers and to establish residence within target host cells. (
  • The small molecule work has also led us to study the molecular mechanisms underlying parasite motility . (
  • Likewise, we have only just begun to understand the molecular mechanisms behind the diverse forms of motility employed by parasites to navigate within their environment. (
  • This study gives molecular clues on B. besnoiti- BAECs interaction and shows the progression of type II endothelial cell activation upon parasite invasion and proliferation. (
  • Parasite cycling within intermediate hosts causes trafficking of molecular epitopes resulting in a generation of parasites variant surface antigens and excretory and/or secretory products that act as host immuno-regulators during co-infections and clinical trials, and hinders the understanding of parasite biology [ 25 - 36 ]. (
  • Therefore, it is not surprising that about 70% of the papers published here deal with early steps of immune responses to protozoan infections, including the role of parasite products, host receptors, molecular mechanisms, and effector cells of innate immune system. (
  • The development of recombinant vaccines is hampered by a relatively poor molecular understanding of the Eimeria -host interface. (
  • We are interested in the cellular and molecular mechanisms that enable apicomplexan parasites to infect and develop inside host. (
  • Heritable mechanisms of refractoriness of the vector that can interrupt several steps of parasite development have been documented, but only recently have modern cell biological, molecular, and genetic approaches been brought to bear on this important topic. (
  • The dearth of molecular insights into mosquito interactions, and our need for such insights should be clear from the accompanying summary of the parasite life history in the mosquito (Robert E. Sinden). (
  • Roos DS (2005) Themes and variations in apicomplexan parasite biology. (
  • Parasitology encompasses the biology, transmission, immunology, epidemiology and control of parasites of veterinary and medical importance. (
  • Our results clearly demonstrate that piggyBac is a novel, indispensable tool for forward functional genomics in P. falciparum that will help better understand parasite biology and accelerate drug and vaccine development. (
  • High throughput methods for identification of gene functions are imperative to better understand parasite biology and develop effective disease control strategies. (
  • as such, probing of the interactions that occur at the host-parasite interface is likely to lead to novel insights into the cell biology underlying leukocyte proliferation and transformation. (
  • Gregarine transcriptome, genome and cell biology data for selected systems will be produced to gain a holistic picture of the gregarine-host-microbiome interactions. (
  • Understanding these processes more deeply will better define the elaborate mechanisms intracellular parasite use to infect their hosts. (
  • Some of these mechanisms resemble those employed for motility in other organisms, while others have features that represent unique adaptations to the demands imposed on a particular parasite. (
  • Mechanisms and outcomes of host-parasite interactions during malaria co-infections with gastrointestinal helminths are reasonably understood. (
  • In contrast, very little is known about such mechanisms in cases of malaria co-infections with tissue-dwelling parasites. (
  • The combined biochemical and cellular assays presented here suggest mechanisms of action for 135 (34%) of the compounds active in killing multiple life-cycle stages of the malaria parasite, including asexual blood, liver, gametocyte, gametes and insect ookinete stages. (
  • Endoparasites have a readily available and renewable supply of nutrients inside the host, which in some cases is pre-digested by the host, so mechanisms of nutrient absorption across their body surface is a common feature. (
  • Our research in medical parasitology spans the spectrum of basic and applied research, from parasite evolution to unraveling resistance mechanisms, and understanding protective immunity in order to develop vaccines. (
  • Our research is revealing the genomic basis to complex disease mechanisms like antigenic variation in trypanosomatid parasites, which cause neglected tropical diseases such as human African trypanosomiasis (sleeping sickness) and leishmaniaisis. (
  • Use of deep sequencing (genomics/transcriptomics) to examine disease mechanisms, virulence factors or antigen discovery in unicellular parasites important to human health (e.g. (
  • Computer structural analysis reveals that azurin shares structural features with the predominant surface antigen SAG1, which is known to play an important role in parasite attachment. (
  • We found that the Cromer blood group antigen CD55 (DAF) is essential for parasite invasion and is necessary for proper attachment of merozoites to the erythrocyte surface. (
  • The apicomplexan parasite Neospora caninum causes neosporosis, a disease that leads to abortion or stillbirth in cattle, generating an economic impact on the dairy and beef cattle trade. (
  • Our results may be helpful to guide the selection of targets to be investigated against Neospora caninum and other Apicomplexan organisms. (
  • rather recently, neospora caninum has been recognized as one of the major protozoal abortion-inducing parasites in cattle. (
  • Despite significant progress in the past decades, how an obligatory IC apicomplexan protozoan parasite, such as Neospora caninum adapts to host cell microenvironment, and the implication of this on the viability of the host cell and the fitness of the parasite remains largely unknown. (
  • Reduced diversity of genes required for host-parasite interaction and transmembrane transport allow hypotheses on host adaptation and specialization of a single host parasite. (
  • These parasites exhibit a remarkable diversity of subcellular organelles, in a stripped-down package facilitating analysis of both common eukaryotic features and novel attributes of interest as therapeutic targets. (
  • The former includes studies on Golgi biogenesis, vesicular trafficking, and cytoskeletal organization, while the latter includes the discovery, biochemical and cell biological characterization of the apicoplast - a nonphotosynthetic plastid acquired when an ancestral parasite 'ate' a eukaryotic alga, and retained the algal plastid (secondary endosymbiosis). (
  • Although this eukaryotic parasite seems able to generate autophagosomes upon stresses such as nutrient starvation, the full functionality and biological relevance of a canonical autophagy pathway are as yet unclear. (
  • Analysis of chromerid algal genomes reveals how apicomplexans have evolved from free-living algae into successful eukaryotic parasites via massive losses and re-inventing functional roles of genes. (
  • However, in contrast to bacteria where the secretion machinery has been resolved in details at the atomic scale, how these eukaryotic parasites secrete and inject rhoptry effectors into cells is still an enigma. (
  • is normally an effective Apicomplexan protozoan with the capacity of infecting any warm-blooded animal worldwide highly. (
  • In this study, we improved efficiency of the piggyBac transposition system for P. falciparum and evaluated its application in whole-genome functional analysis of this most lethal human malaria parasite. (
  • Intriguingly, over 90% of the invasion inhibitors identified in our small molecule screens affect parasite motility. (
  • Although the life cycles of these parasites differ substantially, they share common pathways for actin-myosin-based motility, calcium-dependent secretion, and active cell invasion ( 41 ). (
  • Examples include structural and functional studies of cilia and flagella in paramecia and trypanosomes ( 22 , 68 , 74 ) and of gliding motility in apicomplexan parasites ( 52 ). (
  • This review will discuss biological and mechanistic aspects of cell motility in African trypanosomes, protozoan parasites that are the causative agent of African sleeping sickness. (
  • We will first discuss the importance of trypanosome cell motility for the interaction of the parasite with its mammalian host and insect vector. (
  • Induction of sporozoite motility within the skin is a functionally appropriate physiological response to exposure to albumin upon introduction of sporozoites by mosquitoes into mammalian hosts. (
  • Several interesting complexes were identified in N. caninum tachyzoites and include mitochondrial complexes, proteasome, glideosome and moving junction molecules that play an important role in the physiology and invasion of host cells. (
  • Invasion of host cells allows apicomplexan parasites access to a rich source of nutrients in a niche that is largely protected from host defenses. (
  • Emphasis will be placed on features that are unique to trypanosomes, and for the most part, we will restrict our discussion to Trypanosoma brucei , drawing comparisons to other kinetoplastid parasites where appropriate. (
  • For example, both studies found that the transition from a free-living to parasitic lifestyle was predominantly characterized by gene loss, particularly of genes associated with metabolic function - such as photosynthesis and sterol biosynthesis - suggesting that metabolic pathways that are critical for free-living organisms were lost as apicomplexan parasites evolved towards an intracellular lifestyle. (
  • We further explored the possibility of forward genetic studies in P. falciparum with a phenotypic screen for attenuated growth, which identified several parasite genes and pathways critical for intra-erythrocytic development. (
  • Of the two actin genes in P. falciparum, actin-1 ( pfact1 ) is ubiquitously expressed in all life-cycle stages and is thought to be required for erythrocyte invasion, although its functions during parasite development are unknown, and definitive in vivo characterisation during invasion is lacking. (
  • 8323 genes were annotated with series reads over the two replicating levels from the parasite lifestyle cycle asexually. (
  • The MJ, which is the anchoring structure for the invasion process, is formed by secretion of a macromolecular complex (RON2/4/5/8), derived from secretory organelles called rhoptries, into the host cell membrane. (
  • Apicomplexans enter host cells by the active process of invasion that is driven by the parasite's actin-myosin motor and involves the regulated release of the parasite's specialized secretory organelles (the rhoptries, micronemes and dense granules). (
  • Apicomplexan parasites rely on sequential secretion of specialised secretory organelles for the invasion of the host cell. (
  • This stage invades the host cell in a complex process depending on the parasite's gliding and secretory machinery ( Sibley, 2004 ). (
  • Micronemes are specialized secretory organelles present in all motile forms of apicomplexan parasites. (
  • Now, two studies 1 , 2 compare apicomplexan genomes and transcriptomes with those of closely related free-living algae to explore the genomic changes that underpinned the transition of apicomplexans to parasitism. (
  • B cell activation, proliferation, differentiation and antibody secretion are processes carefully orchestrated by a complex network of intracellular signaling pathways and transcription factors. (
  • The next step in invasion is the recognition of the host cell followed by rhoptry secretion and intimate attachment to the host cell. (
  • Identification of the different elements in the cAMP-dependent signaling pathways that regulate microneme secretion during invasion provides novel targets to block erythrocyte invasion, inhibit blood stage parasite growth and prevent malaria. (
  • Timely secretion of these parasite ligands to the merozoite surface is critical for successful invasion [3] , [4] . (
  • Finally, we show that parasites lacking PfACT1 are capable of microneme secretion, attachment and formation of a junction with the erythrocyte, but are incapable of host cell invasion. (
  • Defining the signaling pathways that lead to microneme secretion is an important part of understanding the infectious cycle of apicomplexan parasites. (
  • The rhoptries are particularly important, because they act as the apicomplexan equivalent of bacterial secretion systems. (
  • To enter cells, they must bind with high affinity to host cell receptors and then uncouple these interactions to complete invasion. (
  • The parasite can then infect these immune cells and use them to disseminate throughout their hosts [ 5 , 6 ]. (
  • Microsporidia are ubiquitous parasites that infect a wide range of animal hosts, and these fungal-related microbes undergo their entire replicative lifecycle inside of host cells. (
  • Despite being widespread in the environment and causing medical and agricultural harm, virtually nothing is known about the host factors important to facilitate their growth and development inside of host cells. (
  • This spore contains a coiled polar tube that can rapidly fire and pierce host cells, and through which a parasite cell called a sporoplasm can be injected directly into a host cell. (
  • All apicomplexan protozoan invasions of host cells are accomplished through matrix-dependent movement, with the force of this movement consisting of actin-myosin complexes located between the parasite's plasma membrane and endometrium [ 6 ]. (
  • Successful expression of fluorescent, luminescent and enzymatic reporters facilitates analysis of transgenic parasites in living cells and animal tissues. (
  • In addition to these metabolic functions, parasite-induced structural changes may alter the interaction of the infected erythrocyte with other host cells and molecules ( 2 , 16 ). (
  • We reported earlier that during chronic toxoplasmosis CD8(+) T cells become functionally exhausted with concomitant PD-1 up-regulation, leading to eventual host mortality. (
  • Tachyzoites propagate rapidly in virtually all types of nucleated cells, including macrophages, while differentiation to bradyzoites is favored in long-lived, terminally differentiated host cells ( 49 ). (
  • Intracellular parasites benefit from the rich resources available inside an infected cell, but they also face the challenges of invading such cells, developing conduits to mine nutrients, and departing their niche on cue. (
  • Population genetic studies dating back to the mid-20th century first proposed that erythrocytes (red blood cells), the host cell for P. falciparum, have been under natural selection due to malaria. (
  • Although the notion that malaria has helped shape the human genome is well- accepted, the lack of a nucleus in human erythrocytes has hindered our ability to study genetic interactions between these unusual host cells and P. falciparum parasites. (
  • Using this approach, we performed a forward genetic screen of human blood groups to identify critical host factors for P. falciparum, and discovered several candidates that appear to be required for efficient parasite invasion of red blood cells. (
  • After an initial multiplication step in liver cells, the parasite invades erythrocytes and multiplies by a process known as schizogony within red blood cells. (
  • In contrast, the invasion of erythrocytes by invasive 'merozoite' forms is a rapid [ 2 - 4 ] and complex process that relies on an orchestrated cascade of interactions between the invading parasite and host cells [ 5 ]. (
  • Excitingly some of these compounds also showed outstanding activity against other disease agents including fungi, bacteria, other single-cellular parasites, worms, and even human cancer cells. (
  • In contrast, in mice chimeric for inducible nitric oxide synthase (iNOS), an enzyme associated with IFN-γ-induced macrophage microbicidal activity, expression by cells of hemopoietic origin was sufficient for host resistance. (
  • Although many possible scenarios have been proposed, these can be distilled into two conceptually distinct "cis" and "trans" models (see Fig. 1 for schematization) that describe how intracellular infections might be controlled within nonmacrophage (i.e., nonhemopoietic) cells. (
  • Intercellular parasites live in spaces within the host e.g. the alimentary canal, whereas intracellular parasites live in cells within the host e.g. erythrocytes. (
  • are a highly successful group of intracellular protozoan parasites that develop within intestinal epithelial cells of poultry, causing coccidiosis. (
  • are a highly successful group of host-specific, intracellular protozoan parasites that develop within intestinal epithelial cells, causing Coccidiosis, which is economically one of the most important diseases in modern poultry farming, and causes billion dollar economic losses worldwide [1] . (
  • The transforming stage of the parasite has a strictly intracellular lifestyle and ensures its distribution to both daughter cells during host cell cytokinesis by aligning itself across the metaphase plate and by binding tightly to central spindle and astral microtubules. (
  • Overall, free cholesterol significantly accumulated in E. bovis infected host cells. (
  • was transfected with C-terminally HA-tagged promoter, inoculated into web host cells, and incubated for 24?h. (
  • Infected MGCD0103 cells typically rupture when they reach 64 to 128 parasites/cell. (
  • Here , we demonstrate that the final step in parasite cell division involves delivery of new plasma membrane to the daughter cells, in a process requiring functional Rab11A . (
  • Second, rhoptries are discharged, leading to the formation of a tight interaction (moving junction) with the host cell, through which the parasite invades. (
  • A number of parasite ligands that mediate receptor binding during invasion reside in apical membrane-bound organelles known as micronemes and rhoptries [1] , [2] . (
  • The surface antigens of apicomplexan parasites function as attachment and invasion in host-parasite interaction. (
  • Inferences from rDNA data are further supported by the several apicomplexan-like structural features in Nephromyces , including especially the strong resemblance of Nephromyces infective stages to apicomplexan sporozoites. (
  • Direct life cycles involve cycling of mature parasites from one definitive host to another while complex life cycles involve cycling of distinct developing life stages through a number of intermediate hosts [ 24 ]. (
  • Analysis of piggyBac insertion sites revealed random insertions into the P. falciparum genome, in regards to gene expression in parasite life cycle stages and functional categories. (
  • piggyBac insertions into the P. falciparum genome were obtained by co-transfection of parasite erythrocytic stages with a transposon plasmid and a transposase-expressing helper plasmid as described previously [ 21 ]. (
  • a pull-down assay has been used to elucidate the binding partners of expressed recombinant GRA2 and GRA7 in both parasites within the host cell lysate. (
  • The differences in the host cell phosphoproteome indicated that these parasites interact with the host cell differently. (
  • However, almost nothing is known about which host cell machinery is important for providing a hospitable host cell environment for microsporidian growth. (
  • Similarly, the availability of extensive libraries of small molecules, host cell cDNAs and siRNA inhibitors, permits complementary reverse- and chemical-genetic approaches. (
  • The parasites can be maintained continuously in vitro in a variety of mammalian cell lines and their requirements for growth have been previously established. (
  • Evidence of active host cell penetration has been presented in scanning electron microscopic studies. (
  • However, such surface observations do not reveal much information on the dynamics of penetration and the manipulation of the host cell by the parasite. (
  • Seemingly unrelated to the catabolic autophagy process, TgATG8 associates with the outer membrane of the nonphotosynthetic plastid harbored by the parasite called the apicoplast, and there it plays an important role in the centrosome-driven inheritance of the organelle during cell division. (
  • Emerging evidence suggests that shifts in available fuel sources and intracellular metabolite concentrations profoundly impact cell fate decisions. (
  • The MTT assay did not reveal any cytotoxic effect of N. caninum challenge on host cell viability. (
  • AMA1 directly mediates the physical interaction between the parasite and host cell: remarkably, the extracellular domain of AMA1 on the parasite surface binds to a receptor on the host cell (RON2) that is inserted into the host cell membrane by the invading parasite. (
  • First, micronemes release their content upon contact with the host cell. (
  • When MIC8 is not present, a block in invasion is caused by the incapability of the parasite to form a moving junction with the host cell. (
  • Because they are obligate intracellular parasites, a key step during their life cycle is the invasion of the host cell. (
  • The complex life cycles of these organisms, generally requiring passage through multiple hosts, as well as the variety of hosts and host tissues that they colonize, provide numerous barriers to cell movement that must be overcome. (
  • Afterwards, expression of surface (CD31, CD34 and CD44) and intracellular markers (vimentin and cytokeratin) was studied to characterize cell populations by flow cytometry. (
  • We raised a phospho-specific antibody and showed that Ser 3233 phosphorylation occurs in the parasite prior to host cell egress. (
  • After the initial attachment of the parasite to the surface of the target cell, the parasite establishes a tight junction between its apical end and the host-cell membrane. (
  • This tight junction progressively moves towards the posterior end of the invading parasite as it enters a red blood cell [ 6 ]. (
  • The sporozoites emerge within the host cell, begin to feed, and develop into larger trophozoites. (
  • Cell-mediated immune responses are critical for immune defense against a variety of intracellular infections as well as tumors. (
  • Here we have used a conditional Cre- lox system to investigate the functions of PfACT1 during P. falciparum blood-stage development and host cell invasion. (
  • Surprisingly, we observe that egress from the host cell is not an actin-dependent process. (
  • The mature schizont undergoes a tightly regulated mechanism of egress to break open the PV and the host cell membranes and release daughter merozoites, thus completing a 48-h asexual cycle. (
  • Given the importance of the parasite surface in maintaining interactions with host microtubules, we analyzed the ultrastructure of the host-parasite interface using transmission electron microscopy combined with high-resolution fluorescence microscopy and live-cell imaging. (
  • The parasites achieve this diversity through a remarkable flexibility of their cell and division cycle. (
  • The lifecycles of apicomplexan parasites are illustrated to highlight the differences in host and cell type specificity. (
  • Eimeria parasites have a single host lifecycle and show a strict tissue and cell type specificity. (
  • Cell host & microbe 23 (3), 302-311. (
  • Consequently they scavenge cholesterol from their host cell apparently in a parasite-specific manner. (
  • Artificial host cell lipid droplet enrichment significantly improved E. bovis merozoite I production confirming the key role of lipid droplet contents for optimal parasite proliferation. (
  • Given that the invading sporozoite stage alone cannot provide all components necessary for this nutrient and energy demanding process, the parasite needs to scavenge molecules from the host cell. (
  • In consequence these parasites scavenge cholesterol from their host cell thereby exploiting different cellular pathways. (
  • Interestingly, different cholesterol auxotrophic parasites appear to follow different strategies of cholesterol scavenge suggesting the modulation of host cell cholesterol metabolism as a parasite-specific and/or host cell-specific process. (
  • Tachyzoites are nevertheless controlled effectively by cell mediated immunity 2,3-DCPE hydrochloride as well as the parasite reverts towards the gradually replicating or quiescent bradyzoite type which resides within tissues cysts that are especially abundant in human brain and heart muscles but may also be present throughout skeletal muscles [3]. (
  • The easily culturable quickly dividing tachyzoite may be the greatest studied type of definitely - there is certainly abundant information regarding cell cycle fat burning capacity and web host parasite interactions because of this stage [6]. (
  • The enterocyte cell level formulated with replicating parasites as proven by IFA (Body?1A) from two 2,3-DCPE hydrochloride parts of the rinsed and opened little intestine were selectively harvested by mechanical stripping (Body?1B). (
  • Cell Host Microbe 19(3):349-360. (
  • Details in the inset show how, in the MJ, AMA1 is exposed on the parasite surface and interacts with a short extracellular domain of RON2 incorporated into the membrane of the host cell. (
  • Ablation of Rab11A function results in daughter parasites having an incompletely formed IMC that leads to a block at a late stage of cell division. (
  • Apicomplexan parasites are unusual in that they replicate by assembling daughter parasites within the mother cell. (
  • They will develop invertebrate cell cultures using tissues from the gut of invertebrate hosts employed in step-1. (
  • This group of obligate parasites evolved from a free-living photosynthetic ancestor (=chromerids) and it is closely related to free living single-cell predators (=colpodellids). (
  • Single cell and subcellular measurement of intracellular Ca2+ concentration ([Ca2+]i). (
  • The infected erythrocytes are subject to an extensive remodeling process induced by the parasite, which facilitates surface exposition of various ligands for host cell receptors, nutrient import into the parasite and asexual reproduction within the host cell. (
  • Host cell remodeling includes the development of electron dense protrusions on the infected red blood cell surface called knobs. (
  • This intracellular part of the asexual life cycle takes 48 h for P. falciparum parasites to complete. (
  • Metabolic reprogramming: an innate cellular defence mechanism against intracellular bacteria? (
  • Whereas recombinant MORN1 produced in bacteria is soluble, in the parasite MORN1 was associated with the cytoskeleton after detergent extraction. (
  • As a result of resistance against anticoccidial drugs and the expense of manufacturing live vaccines, it is necessary to understand the relationship between Eimeria and its host more deeply, with a view to developing recombinant vaccines. (
  • We report a complete genome sequence of the mouse parasite Eimeria falciformis . (
  • Apicomplexans are intracellular parasites and each reproductive cycle is initiated through a motile stage, the zoite. (
  • Infections are initiated by digestion of parasites deposited in cat feces or in undercooked meat. (
  • In most cases, chronic infections are largely asymptomatic unless the host becomes immune compromised. (
  • The development of vaccines against parasitic infections has been complicated due to the fact that co-infecting parasites have life cycles that are either direct or complex. (
  • A great challenge to research in immunology and parasitology is the development of strategies that favor immunity against protozoan parasites and prevent their evasion, chronic, or recurrent infections and associated pathologies. (
  • Macrophage migration inhibitory factor (MIF, " Macrophage migration inhibitory factor in protozoan infections ") is a host inflammatory cytokine with protective or pathogenic actions in distinct protozoan infections. (
  • During 2,3-DCPE hydrochloride severe infections of na?ve intermediate hosts sporozoites from oocysts or bradyzoites from tissues cysts differentiate quickly into tachyzoites which separate rapidly and disseminate through the entire host's body. (
  • 2,3-DCPE hydrochloride That is generally because merozoites aren't cultivatable and tough to gain access to parasite preparations had been generated from enterocytes from an contaminated kitty at starting point of patency (5d post infections). (
  • With respect to worm infections, we study the filarial parasites that cause onchocerciasis (river blindness) and lymphatic filariasis, including major programmes on vaccine development and the function of a bacterial symbiont in these worms ( Wolbachia ), which has become a novel target for antibiotic therapy. (
  • Meanwhile, host immune response is triggered as a result of parasitic invasion. (
  • Occasionally, cysts reactivate and growth of newly emerged parasites must be controlled by the host's immune system or disease will occur. (
  • Bradyzoite conversion is a critical step in the parasite's life cycle since bradyzoites are impervious to immune-mediated destruction, are relatively non-immunogenic, and are the infectious form of the parasite during horizontal transmission (e.g. digestion of undercooked meat). (
  • Host-parasite interactome analysis showed that some DETs were involved in immune signaling, metabolism, biosynthesis-related processes and interspecies interaction. (
  • Applying state-of-the-art imaging techniques to understand interactions between apicomplexan parasites, the intestinal epithelium, and the host immune system in 3D tissue culture models of livestock. (
  • These host proteases might also be important in tissue damage caused by infectious agents, such as in intestinal damage in Clostridium perfringens-induced avian necrotic enteritis (NE). (
  • Apicomplexan parasites divide and replicate through a complex process of internal budding. (
  • Tachyzoites are obligate intracellular parasites that replicate with a duplication time of 6 to 9 hours during growth, depending on strain type. (
  • Upon initial attachment to a surface, the parasite starts to glide in a substrate-dependent manner. (
  • IFA showed that BoTRAP2 is mainly localized on the apical end of parasites by rabbit anti-rBoTRAP2-1 polyclonal serum. (
  • However, the apical polar ring is fragmented in live ΔkinesinAΔapr1 parasites, and is undetectable by electron microscopy after detergent extraction. (
  • Disintegration of the apical polar ring results in the detachment of groups of microtubules from the apical end of the parasite. (
  • For example, when B. bovis invades the host erythrocyte, merozoites first adhere to the RBCs, followed by specific site recognition, invasion, and then asexual multiplication in the invaded RBCs [ 5 ]. (
  • There are three main ways in which blood parasites can be transmitted from an insect vector to a vertebrate host. (
  • Mechanical transmission is characterized by passive transfer of a parasite, specifically on the exterior of the feeding apparatus, into the feeding site on the vertebrate [ 6 ]. (
  • In fact, we are sure there is at least one unique apicomplexan parasite per any invertebrate or vertebrate. (
  • This is contrasted with more extensive knowledge of the vertebrate host. (
  • The parasite grows within erythrocytes, which it invades in a rapid, multistep process. (
  • It can change the structure and function of erythrocytes in host animals, giving rise to the clinical symptoms such as fever, anemia, jaundice, hemoglobinuria and death. (
  • Changes required for intracellular growth are associated with active transport of nutrients from the serum ( 17 ), as well as elimination of catabolites from the parasitized erythrocytes ( 14 ). (
  • These interactions are related to the virulence and transmission strategy of the parasites and so are potentially associated with the biological differences between these parasites. (
  • For other parasites, a tissue invasive phenotype is a key virulence determinant. (
  • Another group conducts research into vector-borne parasites such as African trypanosomes and those causing malaria, focusing on the identification of virulence factors in both laboratory and natural populations. (
  • During the asexual cycle, the parasite interconverts between a fast-growing lytic form known as the tacyhzoite and a slow-growing, semidormant form called the bradyzoite. (
  • The life cycle shows remarkable flexibility between lytic and dormant states, thus facilitating asexual transmission between intermediate hosts. (
  • are intracellular parasites that reside in the cytoplasm of leukocytes. (