A species of gram-negative bacteria in the genus CITROBACTER, family ENTEROBACTERIACEAE. As an important pathogen of laboratory mice, it serves as a model for investigating epithelial hyperproliferation and tumor promotion. It was previously considered a strain of CITROBACTER FREUNDII.
A genus of gram-negative, rod-shaped enterobacteria that can use citrate as the sole source of carbon.
Infections with bacteria of the family ENTEROBACTERIACEAE.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria found in humans and other animals including MAMMALS; BIRDS; REPTILES; and AMPHIBIANS. It has also been isolated from SOIL and WATER as well as from clinical specimens such as URINE; THROAT; SPUTUM; BLOOD; and wound swabs as an opportunistic pathogen.
The segment of LARGE INTESTINE between the CECUM and the RECTUM. It includes the ASCENDING COLON; the TRANSVERSE COLON; the DESCENDING COLON; and the SIGMOID COLON.
A species of gram-negative enterobacteria found in WATER; SEWAGE; SOIL; and FOOD. It can be present in any clinical specimen as an opportunistic pathogen.
Inflammation of the COLON section of the large intestine (INTESTINE, LARGE), usually with symptoms such as DIARRHEA (often with blood and mucus), ABDOMINAL PAIN, and FEVER.
Strains of ESCHERICHIA COLI characterized by attaching-and-effacing histopathology. These strains of bacteria intimately adhere to the epithelial cell membrane and show effacement of microvilli. In developed countries they are associated with INFANTILE DIARRHEA and infantile GASTROENTERITIS and, in contrast to ETEC strains, do not produce ENDOTOXINS.
Pathological processes in the COLON region of the large intestine (INTESTINE, LARGE).
Lining of the INTESTINES, consisting of an inner EPITHELIUM, a middle LAMINA PROPRIA, and an outer MUSCULARIS MUCOSAE. In the SMALL INTESTINE, the mucosa is characterized by a series of folds and abundance of absorptive cells (ENTEROCYTES) with MICROVILLI.
Diseases of rodents of the order RODENTIA. This term includes diseases of Sciuridae (squirrels), Geomyidae (gophers), Heteromyidae (pouched mice), Castoridae (beavers), Cricetidae (rats and mice), Muridae (Old World rats and mice), Erethizontidae (porcupines), and Caviidae (guinea pigs).
Proteins obtained from ESCHERICHIA COLI.
An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.
Physicochemical property of fimbriated (FIMBRIAE, BACTERIAL) and non-fimbriated bacteria of attaching to cells, tissue, and nonbiological surfaces. It is a factor in bacterial colonization and pathogenicity.
The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
A genus of gram-negative, facultatively anaerobic, rod-shaped bacteria whose organisms occur in the lower part of the intestine of warm-blooded animals. The species are either nonpathogenic or opportunistic pathogens.
Measurable quantity of bacteria in an object, organism, or organism compartment.
Cell-surface components or appendages of bacteria that facilitate adhesion (BACTERIAL ADHESION) to other cells or to inanimate surfaces. Most fimbriae (FIMBRIAE, BACTERIAL) of gram-negative bacteria function as adhesins, but in many cases it is a minor subunit protein at the tip of the fimbriae that is the actual adhesin. In gram-positive bacteria, a protein or polysaccharide surface layer serves as the specific adhesin. What is sometimes called polymeric adhesin (BIOFILMS) is distinct from protein adhesin.
Nonsusceptibility to the pathogenic effects of foreign microorganisms or antigenic substances as a result of antibody secretions of the mucous membranes. Mucosal epithelia in the gastrointestinal, respiratory, and reproductive tracts produce a form of IgA (IMMUNOGLOBULIN A, SECRETORY) that serves to protect these ports of entry into the body.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Those components of an organism that determine its capacity to cause disease but are not required for its viability per se. Two classes have been characterized: TOXINS, BIOLOGICAL and surface adhesion molecules that effect the ability of the microorganism to invade and colonize a host. (From Davis et al., Microbiology, 4th ed. p486)
Proteins found in any species of bacterium.
The simplest saturated hydrocarbon. It is a colorless, flammable gas, slightly soluble in water. It is one of the chief constituents of natural gas and is formed in the decomposition of organic matter. (Grant & Hackh's Chemical Dictionary, 5th ed)
A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.
A genus of anaerobic, irregular spheroid-shaped METHANOSARCINALES whose organisms are nonmotile. Endospores are not formed. These archaea derive energy via formation of methane from acetate, methanol, mono-, di-, and trimethylamine, and possibly, carbon monoxide. Organisms are isolated from freshwater and marine environments.
An order of anaerobic methanogens in the kingdom EURYARCHAEOTA. There are two families: METHANOSARCINACEAE and Methanosaetaceae.
A phylum of ARCHAEA comprising at least seven classes: Methanobacteria, Methanococci, Halobacteria (extreme halophiles), Archaeoglobi (sulfate-reducing species), Methanopyri, and the thermophiles: Thermoplasmata, and Thermococci.
An independent state in the Lesser Antilles in the West Indies, north of Venezuela, comprising the islands of Trinidad and Tobago. Its capital is Port of Spain. Both islands were discovered by Columbus in 1498. The Spanish, English, Dutch, and French figure in their history over four centuries. Trinidad and Tobago united in 1898 and were made part of the British colony of Trinidad and Tobago in 1899. The colony became an independent state in 1962. Trinidad was so named by Columbus either because he arrived on Trinity Sunday or because three mountain peaks suggested the Holy Trinity. Tobago was given the name by Columbus from the Haitian tambaku, pipe, from the natives' habit of smoking tobacco leaves. (Webster's New Geographical Dictionary, 1988, p1228, 1216 & Room, Brewer's Dictionary of Names, 1992, p555, 547)
A negatively-charged extracellular matrix protein that plays a role in the regulation of BONE metabolism and a variety of other biological functions. Cell signaling by osteopontin may occur through a cell adhesion sequence that recognizes INTEGRIN ALPHA-V BETA-3.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
Small double-stranded, non-protein coding RNAs, 21-25 nucleotides in length generated from single-stranded microRNA gene transcripts by the same RIBONUCLEASE III, Dicer, that produces small interfering RNAs (RNA, SMALL INTERFERING). They become part of the RNA-INDUCED SILENCING COMPLEX and repress the translation (TRANSLATION, GENETIC) of target RNA by binding to homologous 3'UTR region as an imperfect match. The small temporal RNAs (stRNAs), let-7 and lin-4, from C. elegans, are the first 2 miRNAs discovered, and are from a class of miRNAs involved in developmental timing.
Glycoproteins found on the surfaces of cells, particularly in fibrillar structures. The proteins are lost or reduced when these cells undergo viral or chemical transformation. They are highly susceptible to proteolysis and are substrates for activated blood coagulation factor VIII. The forms present in plasma are called cold-insoluble globulins.
A plant genus of the LAMIACEAE family.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.

Critical role of T cell-dependent serum antibody, but not the gut-associated lymphoid tissue, for surviving acute mucosal infection with Citrobacter rodentium, an attaching and effacing pathogen. (1/177)

Citrobacter rodentium uses virulence factors similar to the enteropathogenic Escherichia coli to produce attaching and effacing lesions in the distal colon of mice. We used this infection model to determine components of adaptive immunity needed to survive infection. During acute infection, wild-type mice develop breaks across infected epithelial surfaces but resolve infection. Surprisingly, mice markedly deficient in mucosal lymphocyte populations from beta(7) integrin deficiency resolve infection, as do CD8alpha-/- or TCR-delta-/- mice. In contrast, CD4-/- or TCR-beta-/- mice develop polymicrobial sepsis and end-organ damage, and succumb during acute infection, despite epithelial damage similar to wild-type mice. B cell-deficient (MuMT-/-) or B and T cell-deficient (recombinase-activating gene 2-/-) mice develop severe pathology in colon and internal organs, and deteriorate rapidly during acute infection. Surviving mice develop robust Citrobacter-specific serum IgM responses during acute infection, whereas mice that succumb do not. However, CD4-/- mice receiving serum Igs from infected wild-type mice survive and clear the infection. Our data show that survival of apparently self-limited and luminal mucosal infections requires a systemic T cell-dependent Ab response against bacteria that enter through damaged mucosa. These findings have implications for understanding host defense against mucosal infections, including the pathogenesis of these diseases in immunocompromised populations.  (+info)

Dissecting virulence: systematic and functional analyses of a pathogenicity island. (2/177)

Bacterial pathogenicity islands (PAI) often encode both effector molecules responsible for disease and secretion systems that deliver these effectors to host cells. Human enterohemorrhagic Escherichia coli (EHEC), enteropathogenic E. coli, and the mouse pathogen Citrobacter rodentium (CR) possess the locus of enterocyte effacement (LEE) PAI. We systematically mutagenized all 41 CR LEE genes and functionally characterized these mutants in vitro and in a murine infection model. We identified 33 virulence factors, including two virulence regulators and a hierarchical switch for type III secretion. In addition, 7 potential type III effectors encoded outside the LEE were identified by using a proteomics approach. These non-LEE effectors are encoded by three uncharacterized PAIs in EHEC O157, suggesting that these PAIs act cooperatively with the LEE in pathogenesis. Our findings provide significant insights into bacterial virulence mechanisms and disease.  (+info)

Identification of a novel Citrobacter rodentium type III secreted protein, EspI, and roles of this and other secreted proteins in infection. (3/177)

Citrobacter rodentium is a member of a group of pathogens that colonize the lumen of the host gastrointestinal tract via attaching and effacing (A/E) lesion formation. C. rodentium, which causes transmissible colonic hyperplasia in mice, is used as an in vivo model system for the clinically significant A/E pathogens enterohemorrhagic and enteropathogenic Escherichia coli. These bacteria all contain a pathogenicity island called the locus of enterocyte effacement (LEE), which encodes a type III secretion system that is designed to deliver effector proteins into eukaryotic host cells. These effectors are involved in the subversion of host eukaryotic cell functions to the benefit of the bacterium. In this study we used mutant strains to determine the effects of the C. rodentium LEE-encoded effectors EspF, EspG, EspH, and Map on virulence in the mouse model. In addition, we identified a novel secreted protein, EspI encoded outside the LEE, whose secretion is also dependent on a functional type III secretion system. Mutant strains with each of the effectors investigated were found to be outcompeted by wild-type bacteria in mixed-infection experiments in vivo, although the effects of EspF and EspH were only subtle. In single-infection experiments, we found that EspF, EspG, and EspH are not required for efficient colonization of the mouse colon or for the production of hyperplasia. In contrast, strains producing EspI and Map had significant colonization defects and resulted in dramatically reduced levels of hyperplasia, and they exhibited very different growth dynamics in mice than the wild-type strain exhibited.  (+info)

Clearance of Citrobacter rodentium requires B cells but not secretory immunoglobulin A (IgA) or IgM antibodies. (4/177)

Citrobacter rodentium, a murine model pathogen for human enteropathogenic Escherichia coli, predominantly colonizes the lumen and mucosal surface of the colon and cecum and causes crypt hyperplasia and mucosal inflammation. Mice infected with C. rodentium develop a secretory immunoglobulin A (IgA) response, but the role of B cells or secretory antibodies in host defense is unknown. To address this question, we conducted oral C. rodentium infections in mice lacking B cells, IgA, secreted IgM, polymeric Ig receptor (pIgR), or J chain. Normal mice showed peak bacterial numbers in colon and feces at 1 week and bacterial eradication after 3 to 4 weeks. B-cell-deficient mice were equally susceptible initially but could not control infection subsequently. Tissue responses showed marked differences, as infection of normal mice was accompanied by transient crypt hyperplasia and mucosal inflammation in the colon and cecum at 2 but not 6 weeks, whereas B-cell-deficient mice had few mucosal changes at 2 weeks but severe epithelial hyperplasia with ulcerations and mucosal inflammation at 6 weeks. The functions of B cells were not mediated by secretory antibodies, since mice lacking IgA or secreted IgM or proteins required for their transport into the lumen, pIgR or J chain, cleared C. rodentium normally. Nonetheless, systemic administration of immune sera reduced bacterial numbers significantly in normal and pIgR-deficient mice, and depletion of IgG abrogated this effect. These results indicate that host defense against C. rodentium depends on B cells and IgG antibodies but does not require production or transepithelial transport of IgA or secreted IgM.  (+info)

Protective role of arginase in a mouse model of colitis. (5/177)

Arginase is the endogenous inhibitor of inducible NO synthase (iNOS), because both enzymes use the same substrate, l-arginine (Arg). Importantly, arginase synthesizes ornithine, which is metabolized by the enzyme ornithine decarboxylase (ODC) to produce polyamines. We investigated the role of these enzymes in the Citrobacter rodentium model of colitis. Arginase I, iNOS, and ODC were induced in the colon during the infection, while arginase II was not up-regulated. l-Arg supplementation of wild-type mice or iNOS deletion significantly improved colitis, and l-Arg treatment of iNOS(-/-) mice led to an additive improvement. There was a significant induction of IFN-gamma, IL-1, and TNF-alpha mRNA expression in colitis tissues that was markedly attenuated with l-Arg treatment or iNOS deletion. Treatment with the arginase inhibitor S-(2-boronoethyl)-l-cysteine worsened colitis in both wild-type and iNOS(-/-) mice. Polyamine levels were increased in colitis tissues, and were further increased by l-Arg. In addition, in vivo inhibition of ODC with alpha-difluoromethylornithine also exacerbated the colitis. Taken together, these data indicate that arginase is protective in C. rodentium colitis by enhancing the generation of polyamines in addition to competitive inhibition of iNOS. Modulation of the balance of iNOS and arginase, and of the arginase-ODC metabolic pathway may represent a new strategy for regulating intestinal inflammation.  (+info)

Macroscopic, microscopic and biochemical characterisation of spontaneous colitis in a transgenic mouse, deficient in the multiple drug resistance 1a gene. (6/177)

1 A novel animal model of spontaneous colonic inflammation, the multiple drug-resistant (mdr1) a(-/-) mouse, was identified by Panwala and colleagues in 1998. The aim of our study was to further characterise this model, specifically by measuring cytokines that have been implicated in inflammatory bowel disease (IBD) (IL-8 and IFN-gamma) in the colon/rectum of mdr1a(-/-) mice, and by determining the sensitivity of these, together with the macroscopic, microscopic and disease signs of colitis, to dexamethasone (0.05, 0.3 and 2 mg kg(-1) subcutaneously (s.c.) daily for 7 days). 2 All mdr1a(-/-) mice had microscopic evidence of inflammation in the caecum and colon/rectum, while control mice with the same genetic background did not. Significant increases in colon/rectum and caecal weights and also in cytokine levels (both IFN-gamma and IL-8) in homogenised colon/rectum were observed in mdr1a(-/-) mice compared to mdr1a(+/+) mice. 3 Dexamethasone reduced the increases in tissue weights and also microscopic grading of colitis severity, but had no effect on IFN-gamma or IL-8. 4 This study supports the similarity of the gastrointestinal inflammation present in mdr1a(-/-) mice to that of human IBD, in particular Crohn's disease. This has been demonstrated at the macroscopic and microscopic levels, and was supported further by elevations in colonic levels of IFN-gamma and IL-8 and the disease signs observed. The incidence of colitis was much higher than previously reported, with all mice having microscopic evidence of colitis. The limited variance between animals in the parameters measured suggests that this model is reproducible.  (+info)

Impaired immunity to intestinal bacterial infection in stromelysin-1 (matrix metalloproteinase-3)-deficient mice. (7/177)

Infection of mice with the intestinal bacterial pathogen Citrobacter rodentium results in colonic mucosal hyperplasia and a local Th1 inflammatory response similar to that seen in mouse models of inflammatory bowel disease. Matrix metalloproteinases (MMPs) have been shown to mediate matrix remodeling and cell migration during tissue injury and repair in the intestine. We have previously shown enhanced pathology in infected TNFRp55-/-, IL-12p40-/-, and IFN-gamma-/- mice, and here we show that this is associated with an increase in stromelysin-1 (MMP3) transcripts in colonic tissues. We have therefore investigated the role of MMP3 in colonic mucosal hyperplasia and the local Th1 responses using MMP3-/- mice. In MMP3-/- mice, similar mucosal thickening was observed after infection as in wild-type (WT) mice. Colonic tissues from MMP3-/- mice showed a compensatory increase in the expression of other MMP transcripts, such as MMP7 and MMP12. However, MMP3-/- mice showed delayed clearance of bacteria and delayed appearance of CD4+ T lymphocytes into intestinal lamina propria. CSFE-labeled mesenteric lymph node CD4+ T lymphocytes from infected WT mice migrated in fewer numbers into the mesenteric lymph nodes and colon of MMP3-/- mice than into those of WT mice. These studies show that mucosal remodeling can occur in the absence of MMP3, but that MMP3 plays a role in the migration of CD4+ T lymphocytes to the intestinal mucosa.  (+info)

EspJ is a prophage-carried type III effector protein of attaching and effacing pathogens that modulates infection dynamics. (8/177)

Enterohemorrhagic Escherichia coli, enteropathogenic E. coli, and Citrobacter rodentium are highly adapted enteropathogens that successfully colonize their host's gastrointestinal tract via the formation of attaching and effacing (A/E) lesions. These pathogens utilize a type III secretion system (TTSS) apparatus, encoded by the locus of enterocyte effacement, to translocate bacterial effector proteins into epithelial cells. Here, we report the identification of EspJ (E. coli-secreted protein J), a translocated TTSS effector that is carried on the 5' end of the cryptic prophage CP-933U. Infection of epithelial cells in culture revealed that EspJ is not required for A/E lesion activity in vivo and ex vivo. However, in vivo studies performed with mice demonstrated that EspJ possesses properties that influence the dynamics of clearance of the pathogen from the host's intestinal tract, suggesting a role in host survival and pathogen transmission.  (+info)

TY - JOUR. T1 - Enhanced susceptibility to Citrobacter rodentium infection in microRNA-155-deficient mice. AU - Clare, Simon. AU - John, Victoria. AU - Walker, Alan W. AU - Hill, Jennifer L. AU - Abreu-Goodger, Cei. AU - Hale, Christine. AU - Goulding, David. AU - Lawley, Trevor D. AU - Mastroeni, Pietro. AU - Frankel, Gadi. AU - Enright, Anton J. AU - Vigorito, Elena. AU - Dougan, Gordon. PY - 2013/3. Y1 - 2013/3. N2 - MicroRNAs (miRNAs) are small noncoding molecules that control gene expression posttranscriptionally, with microRNA-155 (miR-155) one of the first to be implicated in immune regulation. Here, we show that miR-155-deficient mice are less able to eradicate a mucosal Citrobacter rodentium infection than wild-type C57BL/6 mice. miR-155-deficient mice exhibited prolonged colonization associated with a higher C. rodentium burden in gastrointestinal tissue and spread into systemic tissues. Germinal center formation and humoral immune responses against C. rodentium were severely impaired ...
The intestinal epithelial cells (IECs) that line the gut form a robust line of defense against ingested pathogens. We investigated the impact of infection with the enteric pathogen Citrobacter rodentium on mouse IEC metabolism using global proteomic and targeted metabolomics and lipidomics. The major signatures of the infection were upregulation of the sugar transporter Sglt4, aerobic glycolysis, and production of phosphocreatine, which mobilizes cytosolic energy. In contrast, biogenesis of mitochondrial cardiolipins, essential for ATP production, was inhibited, which coincided with increased levels of mucosal O2 and a reduction in colon-associated anaerobic commensals. In addition, IECs responded to infection by activating Srebp2 and the cholesterol biosynthetic pathway. Unexpectedly, infected IECs also upregulated the cholesterol efflux proteins AbcA1, AbcG8, and ApoA1, resulting in higher levels of fecal cholesterol and a bloom of Proteobacteria. These results suggest that C. rodentium ...
Murphy, CT, Hall, LJ, Hurley, G, Quinlan, A, MacSharry, J, Shanahan, F, Nally, K and Melgar, S (2012) The Sphingosine-1-Phosphate Analogue FTY720 Impairs Mucosal Immunity and Clearance of the Enteric Pathogen Citrobacter rodentium. Infection and Immunity, 80 (8). pp. 2712-2723. ISSN 0019-9567 Full text not available from this repository. (Request a copy ...
The human pathogens enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC), as well as the mouse pathogen Citrobacter rodentium encode type III secretion system (T3SS) effector proteins to promote their survival in the infected host. The mechanisms of action and the host targets of T3SS effectors are under active investigation because of their importance to bacterial virulence. The non-locus of enterocyte effacement (LEE)-encoded protein F, NleF, contributes to E. coli and C. rodentium colonization of piglets and mice, respectively. Here we sought to characterize the host binding partners of NleF. Using a yeast two-hybrid screen, we identified Tmp21, a type-I integral membrane protein and COPI-vesicle receptor involved in trans-Golgi network function, as an NleF-binding partner. We confirmed this interaction using immunoprecipitation and bimolecular fluorescence complementation (BiFC). We expressed a temperature-sensitive vesicular stomatitis virus glycoprotein (tsVSVG) to ...
TY - JOUR. T1 - Osteopontin mediates Citrobacter rodentium-induced colonic epithelial cell hyperplasia and attaching-effacing lesions. AU - Wine, Eytan. AU - Shen-Tu, Grace. AU - Gareau, Melanie. AU - Goldberg, Harvey A.. AU - Licht, Christoph. AU - Ngan, Bo Yee. AU - Sorensen, Esben S.. AU - Greenaway, James. AU - Sodek, Jaro. AU - Zohar, Ron. AU - Sherman, Philip M.. PY - 2010/9. Y1 - 2010/9. N2 - Although osteopontin (OPN) is up-regulated in inflammatory bowel diseases, its role in disease pathogenesis remains controversial. The objective of this study was to determine the role of OPN in host responses to a non-invasive bacterial pathogen, Citrobacter rodentium, which serves as a murine infectious model of colitis. OPN gene knockout and wild-type mice were infected orogastrically with either C. rodentium or Luria-Bertani (LB) broth. Mouse-derived OPN+/+ and OPN-/- fibroblasts were incubated with C. rodentium and attachingeffacing lesions were demonstrated using transmission electron ...
Infection with Citrobacter rodentium triggers robust tissue damage repair responses, manifested by secretion of IL-22, in the absence of which mice succumbed
In this report we have added to our understanding of the role of ILK in intestinal pathophysiology, specifically in the setting of bacterial infection. Similar to the findings reported for DSS-induced colitis we show that there is a reduced inflammatory response, associated with a reduction in CCL2 expression, an important immune cell chemoattractant. Furthermore, our findings indicate that the pattern but not the magnitude of epithelial C. rodentium binding is altered in the ILK-ko mice, with preserved apical binding but reduced lateral epithelial cell binding/migration, in between adjacent crypts. Although the reduced expression of fibronectin may account for this finding, we cannot exclude alterations in other extracellular matrix components, or alterations in the levels of other cell surface integrins as being involved in this response. An additional role for ILK is indicated by the reduced crypt hyperplasia observed associated with decreased cyclin D1 on immunohistochemistry, in ILK-ko ...
Macrophages play pleiotropic roles in maintaining the balance between immune tolerance and inflammatory responses in the gut. Here, we identified transcription factor RBP-J as a crucial regulator of colonic macrophage-mediated immune responses against the enteric pathogen Citrobacter rodentium . In the immune response phase, RBP-J promoted pathogen clearance by enhancing intestinal macrophage-elicited Th17 cell immune responses, which was achieved by maintenance of C/EBPβ-dependent IL-6 production by overcoming miRNA-17∼92-mediated suppressive effects. RBP-J deficiency-associated phenotypes could be genetically corrected by further deleting miRNA-17∼92 in macrophages. In the late phase, noneradicated pathogens in RBP-J KO mice recruited abundant IL-1β-expressing CD64 + Ly6C + colonic macrophages and thereby promoted persistence of ILC3-derived IL-22 to compensate for the impaired innate and adaptive immune responses, leading to ultimate clearance of pathogens. These results demonstrated ...
Enteropathogenic E. coli (EPEC), Enterohaemorhagic E. coli (EHEC) and Citrobacter rodentium are constituent members of the attaching and effacing (A/E) pathogens. The A/E group of bacteria are considered to be extracellular pathogens which form characteristic lesions by intimately adhering to host enterocytes and directing the effacement intestinal brush border. EPEC and EHEC are diarrhoeal pathogens, which are a global health burden in developing and industrialised countries respectively. Citrobacter rodentium is a murine pathogen which is an excellent animal model for EPEC and EHEC infection. EPEC, EHEC and C. rodentium conserve a genomic region termed the locus of enterocyte effacement (LEE) which encodes a type 3 secretion system (T3SS), a core set of type 3 secreted effector proteins and the outer membrane adhesin intimin, which are essential for A/E lesion formation. A/E pathogens utilise their T3SSs to translocate dozens of effector proteins directly from the bacteria into host cells. ...
AB - Tracking disease progression in vivo is essential for the development of treatments against bacterial infection. Optical imaging has become a central tool for in vivo tracking of bacterial population development and therapeutic response. For a precise understanding of in vivo imaging results in terms of disease mechanisms derived from detailed postmortem observations, however, a link between the two is needed. Here, we develop a model that provides that link for the investigation of Citrobacter rodentium infection, a mouse model for enteropathogenic Escherichia coli (EPEC). We connect in vivo disease progression of C57BL/6 mice infected with bioluminescent bacteria, imaged using optical tomography and X-ray computed tomography, to postmortem measurements of colonic immune cell infiltration. We use the model to explore changes to both the host immune response and the bacteria and to evaluate the response to antibiotic treatment. The developed model serves as a novel tool for the ...
Background: Transmaternal exposure to tobacco, microbes, nutrients, and other environmental factors shapes the fetal immune system through epigenetic processes. The gastric microbe Helicobacter pylori represents an ancestral constituent of the human microbiota that causes gastric disorders on the one hand and is inversely associated with allergies and chronic inflammatory conditions on the other. Objective: Here we investigate the consequences of transmaternal exposure to H pylori in utero and/or during lactation for susceptibility to viral and bacterial infection, predisposition to allergic airway inflammation, and development of immune cell populations in the lungs and lymphoid organs. Methods: We use experimental models of house dust mite- or ovalbumin-induced airway inflammation and influenza A virus or Citrobacter rodentium infection along with metagenomics analyses, multicolor flow cytometry, and bisulfite pyrosequencing, to study the effects of H pylori on allergy severity and immunologic ...
Authors: Vidhya Vijayakumar, Araceli Santiago, Rachel Smith, Mark Smith, Roy M Robins-Browne, James P Nataro, Fernando Ruiz-Perez
The taking a chances that diarrhea clears intestinal pathogens has been weighed for centuries, protested corresponding originator Jerrold Turner, MD, PhD, of the BWH Regions of Pathology and Nostrum. Its colliding on the gaining headway of intestinal infections residua poorly agreed. We sought to set down the task of diarrhea and to see if anticipating it influence really wait pathogen interruption and prolong evil.. To delve into, researchers fit of pique to a mouse mannequin infected with Citrobacter rodentium, the mouse a tender-hearted of an E. coli infection. Enervating this after, they saw an add to in the permeability of the intestinal ditch within well-founded two periods of infection - away ahead of redness and epithelial impairment. In particular, they uncovered a speculative role for interleukin-22 that in energize influences another molecule reasoned claudin-2, beforehand conscious to be embroiled with in provoking diarrhea. They secure that diarrhea impacting from the signaling ...
The rapid turnover and exfoliation of mucosal epithelial cells provides an innate defence system against bacterial infection. Nevertheless, many pathogenic bacteria, including Shigella, are able to surmount exfoliation and colonize the epithelium efficiently. Here we show that the Shigella flexneri effector OspE (consisting of OspE1 and OspE2 proteins), which is highly conserved among enteropathogenic Escherichia coli, enterohaemorrhagic E. coli, Citrobacter rodentium and Salmonella strains, reinforces host cell adherence to the basement membrane by interacting with integrin-linked kinase (ILK). The number of focal adhesions was augmented along with membrane fraction ILK by ILK-OspE binding. The interaction between ILK and OspE increased cell surface levels of beta1 integrin and suppressed phosphorylation of focal adhesion kinase and paxillin, which are required for rapid turnover of focal adhesion in cell motility. Nocodazole-washout-induced focal adhesion disassembly was blocked by expression ...
TY - JOUR. T1 - NIK signaling axis regulates dendritic cell function in intestinal immunity and homeostasis. AU - Jie, Zuliang. AU - Yang, Jin Young. AU - Gu, Meidi. AU - Wang, Hui. AU - Xie, Xiaoping. AU - Li, Yanchuan. AU - Liu, Ting. AU - Zhu, Lele. AU - Shi, Jianhong. AU - Zhang, Lingyun. AU - Zhou, Xiaofei. AU - Joo, Donghyun. AU - Brightbill, Hans D.. AU - Cong, Yingzi. AU - Lin, Daniel. AU - Cheng, Xuhong. AU - Sun, Shao Cong. PY - 2018/1/1. Y1 - 2018/1/1. N2 - Dendritic cells (DCs) play an integral role in regulating mucosal immunity and homeostasis, but the signaling network mediating this function of DCs is poorly defined. We identified the noncanonical NF-κB-inducing kinase (NIK) as a crucial mediator of mucosal DC function. DC-specific NIK deletion impaired intestinal immunoglobulin A (IgA) secretion and microbiota homeostasis, rendering mice sensitive to an intestinal pathogen, Citrobacter rodentium. DC-specific NIK was required for expression of the IgA transporter polymeric ...
Bacteria have mechanisms to export proteins for diverse purposes, including colonization of hosts and pathogenesis. A small number of archetypal bacterial secretion machines have been found in several groups of bacteria and mediate a fundamentally distinct secretion process. Perhaps erroneously, proteins called autotransporters have long been thought to be one of these protein secretion systems. Mounting evidence suggests that autotransporters might be substrates to be secreted, not an autonomous transporter system. We have discovered a new translocation and assembly module (TAM) that promotes efficient secretion of autotransporters in proteobacteria. Functional analysis of the TAM in Citrobacter rodentium, Salmonella enterica and Escherichia coli showed that it consists of an Omp85-family protein, TamA, in the outer membrane and TamB in the inner membrane of diverse bacterial species. The discovery of the TAM provides a new target for the development of therapies to inhibit colonization by ...
To investigate, researchers used a mouse model infected with Citrobacter rodentium, the mouse equivalent of an E. coli infection. Using this model, they saw an increase in the permeability of the intestinal barrier within just two days of infection -- well before inflammation and epithelial damage. In particular, they uncovered a critical role for interleukin-22 that in turn influences another molecule called claudin-2, previously known to be involved in causing diarrhea. They found that diarrhea resulting from the signaling of these two molecules helped promote pathogen clearance and limited disease severity ...
The twin-arginine translocation (Tat) system is involved in not only a wide array of cellular processes but also pathogenesis in many bacterial pathogens; thus, this system is expected to become a novel therapeutic target to treat infections. To the best of our knowledge, involvement of the Tat system has not been reported in the gut infection caused by Citrobacter rodentium. Here, we studied the... ...
Bruce A. Vallance is the author of these articles in the Journal of Visualized Experiments: The Citrobacter rodentium Mouse Model: Studying Pathogen and Host Contributions to Infectious Colitis, DNBS/TNBS Colitis Models: Providing Insights Into Inflammatory Bowel Disease and Effects of Dietary Fat
The TH17 cell, a third subset of effector T helper cells, is the subject of intense research to understand their role in immunity and disease. An excellent review of emerging data suggests that the TH17 cells have an important role in host defense against specific pathogens, some of which include Propionibacterium acnes, the Gram-negative Citrobacter rodentium, Klebsiella pneumoniae, Bacteroides spp. and Borrelia spp., the acid-fast Mycobacterium tuberculosis, and fungi such as Candida albicans. They are also potent inducers of autoimmunity and tissue inflammation. In addition, differentiation factors responsible for TH17 generation reveal an interesting reciprocal relationship with regulatory T (Treg) cells, which prevent tissue inflammation and mediate self-tolerance. Editors comment: A fantastic review of a subject of interest to all allergists/immunologists. A must read. Bettelli E, et al., Nature 2008; ...
There are no previous reports on whether the presence or absence of epinephrine and norepinephrine affects the composition of the gut microbiota. Because the virulence and infectivity of EHEC and C. rodentium are altered by the microbiota (64, 67-69) and because the microbiota plays an important role in the availability of active epinephrine and/or norepinephrine in the lumen (5), we investigated the compositions of the microbiotas of uninfected and infected Dbh+/− and Dbh−/− animals at the phylum level. The compositions were similar on day 1 of C. rodentium infection (Fig. 5A). At day 7, the uninfected animals had microbiotas that were similar to those of each other and to their microbiotas prior to infection (Fig. 5B). Infection of Dbh+/− and Dbh−/− mice resulted in changes in the microbiota with all strains. However, these changes differed depending on whether these animals were or were not able to produce epinephrine and norepinephrine. At day 7, in animals infected with WT C. ...
Taconic produces mice and rats at multiple health standards that meet specific research requirements. These health standards range from the most stringent Germ Free (GF) health standards to Murine Pathogen Free (MPF) where a select list of opportunistic bacteria are tolerated.
Teaching Files with CT Medical Imaging and case studies on Anatomical Regions including Adrenal, Colon, Cardiac, Stomach, Pediatric, Spleen, Vascular, Kidney, Small Bowel, Liver, Chest | CTisus
Host fucosylation increases tolerance of a pathogena, Difference in % weight loss between LPS-injected C. rodentium-infected and uninfected mice (mean±s.e.m.;
Looking for online definition of Pneumospirura rodentium in the Medical Dictionary? Pneumospirura rodentium explanation free. What is Pneumospirura rodentium? Meaning of Pneumospirura rodentium medical term. What does Pneumospirura rodentium mean?
Methane is metabolized principally by methanotrophs and methanogens in the global carbon cycle. Methanotrophs consume methane as the only source of carbon, while methanogens produce methane as a metabolic byproduct. Methylotrophs, which are microorganisms that can obtain energy for growth by oxidizing one-carbon compounds, such as methanol and methane, are situated between methanotrophs and methanogens. Methanogens can obtain energy for growth by converting a limited number of substrates to methane under anaerobic conditions. Three types of methanogenic pathways are known: CO2 to methane [MD:M00567], methanol to methane [MD:M00356], and acetate to methane [MD:M00357]. Methanogens use 2-mercaptoethanesulfonate (CoM; coenzyme M) as the terminal methyl carrier in methanogenesis and have four enzymes for CoM biosynthesis [MD:M00358]. Coenzyme B-Coenzyme M heterodisulfide reductase (Hdr), requiring for the final reaction steps of methanogenic pathway, is divided into two types: cytoplasmic HdrABC in ...
Leukocyte Adhesion Deficiency type I (LAD-I) is a primary immune deficiency caused by mutations in the CD18 subunit of β2 integrins. Affected individuals suffer from recurrent mucocutaneous infections and pathologic inflammation in certain mucosal barriers, including the periodontium, skin and the colon. Our laboratory has recently dissected the mechanistic basis of LAD-I-associated periodontitis but the mechanisms underlying LAD-I- associated colitis are yet to be defined. To answer this question, we utilized as model the CD18−/− mice after demonstrated that CD18 deficiency renders mice highly susceptible to Citrobacter rodentium-induced colitis, a widely used model of human colitis caused by enteropathogenic and enterohaemorrhagic Escherichia coli. Strikingly, we found that CD18−/− mice displayed significantly reduced IL-22 production and IL-22 producing Group 3 innate lymphoid cells (ILC3s). Therapeutic delivery of recombinant IL-22 (rIL-22) protected CD18−/− mice from C. ...
ID D2THD2_CITRI Unreviewed; 317 AA. AC D2THD2; DT 02-MAR-2010, integrated into UniProtKB/TrEMBL. DT 02-MAR-2010, sequence version 1. DT 25-OCT-2017, entry version 48. DE RecName: Full=2-keto-3-deoxygluconate permease {ECO:0000256,HAMAP-Rule:MF_00070}; DE Short=KDG permease {ECO:0000256,HAMAP-Rule:MF_00070}; GN Name=kdgT {ECO:0000256,HAMAP-Rule:MF_00070}; GN OrderedLocusNames=ROD_01271 {ECO:0000313,EMBL:CBG86907.1}; OS Citrobacter rodentium (strain ICC168) (Citrobacter freundii biotype OS 4280). OC Bacteria; Proteobacteria; Gammaproteobacteria; Enterobacterales; OC Enterobacteriaceae; Citrobacter. OX NCBI_TaxID=637910 {ECO:0000313,EMBL:CBG86907.1, ECO:0000313,Proteomes:UP000001889}; RN [1] {ECO:0000313,EMBL:CBG86907.1, ECO:0000313,Proteomes:UP000001889} RP NUCLEOTIDE SEQUENCE [LARGE SCALE GENOMIC DNA]. RC STRAIN=ICC168 {ECO:0000313,EMBL:CBG86907.1, RC ECO:0000313,Proteomes:UP000001889}; RX PubMed=19897651; DOI=10.1128/JB.01144-09; RA Petty N.K., Bulgin R., Crepin V.F., Cerdeno-Tarraga A.M., RA ...
Enteropathogenic E. coli (EPEC) is a major public health concern in developing countries where it causes significant morbidity and mortality in infants. EPEC, along with a few other related pathogens namely enterohemorrhagic E. coli (EHEC), Citrobacter rodentium, rabbit enteropathogenic E. coli (REPEC), and Escherichia albertii constitute a group collectively referred to as attaching and effacing (A/E) pathogens. They are so called because upon infection these pathogens attach intimately to intestinal cells and destroy cellular microvilli. Destruction of the microvilli reduces the ability of the cells to absorb water and nutrients, which ultimately leads to diarrhea. Upon destruction, the infected bacterium recruits the structural proteins from the microvilli and remodels them to form filament-like protrusions that extend out of the infected cell and are crowned on top by the infecting bacterium (Fig. 1). This histopathological structure is commonly referred to as attaching and effacing (A/E) ...
First, a number of transcripts had distinct transcriptional activity between the two lines of mice at all time points. For example, FVB mice had consistently four- to eight-fold higher expression of the adenosine A2B receptor gene (Adora2b).. Second, a group of genes, although consistently overexpressed in FVB mice compared to SW mice, also exhibited different expression as a function of time during infection. The Sorting nexin gene (Snx6; overexpressed in FVB mice by 16- to 31-fold compared with SW mice) had increased expression at 4 dpi by approximately 2-fold in both lines of mice. However, at 9 dpi, expression of Snx6 remained elevated in FVB mice, but returned to normal in SW mice. Another example was proton-dependent high affinity oligopeptide transporter Pept2 (Slc15a2), which was overexpressed in FVB mice by 15- to 51-fold. Slc15a2 was upregulated in infected SW mice by 2-fold at 4 dpi and downregulated by 4-fold at 9 dpi, whereas in infected FVB mice its expression decreased by 11-fold ...
The Tagbilaran Maternity and Childrens Hospital (TMCH) was temporarily closed starting Monday after a child who was identified as a contact of a COVID-19 positive person was admitted at the hospital without full disclosure of his exposure. According to TMCH medical director Dr. Lester Balagonsa
Citrobacter farmeri is a Gram-negative species of bacteria. Brenner, D. J.; Grimont, P. A. D.; Steigerwalt, A. G.; Fanning, G. R.; Ageron, E.; Riddle, C. F. (1993). Classification of Citrobacteria by DNA Hybridization: Designation of Citrobacter farmeri sp. nov., Citrobacter youngae sp. nov., Citrobacter braakii sp. nov., Citrobacter werkmanii sp. nov., Citrobacter sedlakii sp. nov., and Three Unnamed Citrobacter Genomospecies. International Journal of Systematic Bacteriology. 43 (4): 645-658. doi:10.1099/00207713-43-4-645. ISSN 0020-7713. PMID 8240948. Tan, C. K.; Lai, C. C.; Lin, S. H.; Liao, C. H.; Huang, Y. T.; Hsueh, P. R. (2010). Fatal Citrobacter farmeri Meningitis in a Patient with Nasopharyngeal Cancer. Journal of Clinical Microbiology. 48 (4): 1499-1500. doi:10.1128/JCM.00282-10. ISSN 0095-1137. PMC 2849549 . PMID 20181904. Bruckner DA, Colonna P, Glenn D, Abbott SL, Janda JM (1997). Citrobacter farmeri bacteremia in a child with short-bowel syndrome. J Clin Microbiol. 35 (12): ...
The microbes that piqued Pitouts interest were common intestinal-dwelling bacteria that harbored special. to be the worlds third-biggest air travel market by 2035. Since Pitout noted the infection link, the South Asian nation has come.. Acute diarrhea is most commonly due to viral gastroenteritis with rotavirus, which accounts for 40% of cases in children under five. In travelers, however, bacterial.. The stool culture is a test that allows the detection and identification of pathogenic bacteria in the stool. In the laboratory, a small amount of a fresh faecal.. Surf Camp In Nicaragua Nicaragua Real Estate For Sale, Affortable and Luxury Real Estate, For Sale By Owner, Realtors, Agents and Brokers. We have become a virtual refugee camp, right here in the heart of San Diego, said. We lost all hope, because it was truly. Well work on those charts later. (Additional info below color wheel) Made from bile when iron of red blood cells mixes with broken down bone marrow, turned brown by bacteria ...
Citrobacter freundii appear as Gram-negative, rod-shaped bacteria that are 0.3-1 micrometer in diameter and 0.6-6 micrometers in length. Citrobacter have hair-like extensions, called flagella, that...
do you know any links/sites i can use as a reference or any info on citrobacter freundii that are scientific resources? im doing a microbiology research profile ...
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Fevers associated with inflammation of the colon and rectum, such as infectious colitis, may also contribute to a burning sensation during bowel movements. Characterized by small tears found on the lining of the anus mucosa that cause severe pain when passing stool.. I went to a gastroenterologist, had an endoscopy done and was once again diagnosed with GERD. This time the outcome has not been so good. The GI doctor I saw prescribed two different medications. I was having bad reaction to the medicine and felt the only thing the GI doctor was doing was medicating me.. I have no idea what triggered it off but it is awful all day apart from first thing in the morning. Then as soon as the day goes on it creeps up and gets worse and worse. I have tried avoiding all the usual triggers and have also had 2 very unsuccessful attempts on PPIs. After trying the first for 3 weeks I stopped as there was no change at all and it ended up making me feel worse.. No statement herein is to be construed as a ...
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Enterohemorrhagic E. coli (EHEC) is an important subset of Shiga toxin-producing (Stx-producing) E. coli (STEC), pathogens that have been implicated in outbreaks of food-borne illness and can cause intestinal and systemic disease, including severe renal damage. Upon attachment to intestinal epithelium, EHEC generates attaching and effacing (AE) lesions characterized by intimate attachment and actin rearrangement upon host cell binding. Stx produced in the gut transverses the intestinal epithelium, causing vascular damage that leads to systemic disease. Models of EHEC infection in conventional mice do not manifest key features of disease, such as AE lesions, intestinal damage, and systemic illness. In order to develop an infection model that better reflects the pathogenesis of this subset of STEC, we constructed an Stx-producing strain of Citrobacter rodentium, a murine AE pathogen that otherwise lacks Stx. Mice infected with Stx-producing C. rodentium developed AE lesions on the intestinal epithelium
Citrobacter freundi is a species of facultative. aerobic. Gram-negative bacilli of the Enterobacteriaceae family.[4] The bacteria are long rod-shaped with a typical length of 1-5 μm.[5] Most C. freundii cells are surrounded by several flagella used for locomotion, but a few are not mobile. It can be found in soil, water, sewage, food, and the intestinal tracts of animals and humans.[5] The Citrobacter genus was discovered in 1932 by Werkman and Gillen. Cultures of C. freundii were isolated and identified in the same year from soil extracts.[5] ...
Results No behavioural abnormalities were observed, either at the height of infection (10 days) or following bacterial clearance (30 days), in C rodentium-infected C57BL/6 mice. When infected mice were exposed to acute stress, however, memory dysfunction was apparent after infection (10 days and 30 days). Memory dysfunction was prevented by daily treatment of infected mice with probiotics. Memory was impaired in germ-free mice, with or without exposure to stress, in contrast to conventionally reared, control Swiss-Webster mice with an intact intestinal microbiota. ...
The digestive tract or the gastrointestinal tract is filled with muscle that passes foods through the small intestines to the colon. If you are healthy and there is no health disruption present, these muscular activities along the digestive tracts will sweep the foods from the stomach into the colon properly, in that all the bacteria present are also sweep through to its final site, the colon. Some conditions, though, may be responsible for improper or insufficient muscular activities that result in the inability of these muscles to sweep the foods and bacteria to the colon. Instead, there is some bacteria leftover in the small intestines. The presence of these bacteria increases your risk of having intestinal bacterial infection.. There are some conditions which contribute to abnormal muscular activity in your digestive tracts, such as:. ...
This study aimed to investigated the prevalence and resistance pattern of different Citrobacter species phenotypically and genotypically to β-lactam and some most common antibiotics then evaluate the antibacterial activity of omega-3 extracted from flaxseed against isolates that harboring resistance genes. 19 Citrobacter isolates were isolated from100 stool and urine samples taken from patients attended to AL-Sadar Hospital during June-December 2016. Clinical samples were cultured on specific media, thereafter isolates were identified depending on morphological, biochemical characteristics and VITK-2. The results showed that the Citrobacter comprise 24% of isolated bacteria which divided into 11 (14.1%) were C. freundii, 5 (6.41%) C. kosaeri and C. farmeri were 3 (3.8%). The antagonistic activity was evaluated by observing a clear zone of inhibition growth, the results showed that all Citrobacter (100%) isolates were resistant to Ampicillin, cefoxitin and sensitive to Imipinim, also the ...
Mono- and Stereopictres of 5.0 Angstrom coordination sphere of Arsenic atom in PDB 3bfd: Crystal Structure of the Class A Beta-Lactamase Sed-G238C Mutant From Citrobacter Sedlakii
In this Review, we discuss recent studies in which C. rodentium has been used to study mucosal immunology, including the deregulation of intestinal inflammatory responses during bacteria-induced colitis and the role of the intestinal microbiota ...
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p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class=publication>Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href=http://www.nrbook.com/b/bookcpdf.php>Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
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Citrobacter is a genus of Gram-negative coliform bacteria in the Enterobacteriaceae family. The species C. amalonaticus, C. koseri, and C. freundii can use citrate as a sole carbon source. Citrobacter species are differentiated by their ability to convert tryptophan to indole (C. koseri is the only citrobacter to be commonly indole-positive), ferment lactose (C. koseri is a non-lactose fermentor), and use malonate. Citrobacter shows the ability to accumulate uranium by building phosphate complexes. These bacteria can be found almost everywhere in soil, water, wastewater, etc. They can also be found in the human intestine. They are rarely the source of illnesses, except for infections of the urinary tract and infant meningitis and sepsis. C. freundii strains have inducible ampC genes encoding resistance to ampicillin and first-generation cephalosporins. In addition, isolates of Citrobacter may be resistant to many other antibiotics as a result of plasmid-encoded resistance genes. LPSN ...
Oct. 11, 2017 - Studies from Dr. Feng Shaos laboratory reveals a novel ubiquitination and degradation mechanism used by an enteric bacterial pathogen Shigella flexneri to counteract cell-autonomous innate immune defense. The work entitled
Inflammatory bowel disease (IBD) is thought to result from either an abnormal immunological response to enteric flora or a normal immunological response to a specific pathogen. No study to date has combined both factors. The present studies were carried out with an immunologically manipulated mouse model of IBD. Mice homozygous for the severe combined immunodeficiency (scid) mutation develop IBD with adoptive transfer of CD4+ T cells expressing high levels of CD45RB (CD45RB(high) CD4+ T cells). These mice do not develop IBD in germfree conditions, implicating undefined intestinal flora in the pathogenesis of lesions. In controlled duplicate studies, the influence of a single murine pathogen, Helicobacter hepaticus, in combination with the abnormal immunological response on the development of IBD was assessed. The combination of H. hepaticus infection and CD45RB(high) CD4+ T-cell reconstitution resulted in severe disease expression similar to that observed in human IBD. This study demonstrates ...
In an attempt to clarify the complex nature of interactions between the cortical actin cytoskeleton and integral membrane proteins, recent studies brought into focus the ERM proteins, which serve as cross-linkers between specific plasma membrane proteins and cortical actin filaments. For ERM protein activation, specific signals, such as phosphorylation or binding of phosphatidylinositol 4,5-bisphosphate (lipid signaling molecule) to the N-terminal domain is required (8, 25, 36). Activation of ERM proteins may be triggered by physiological (14, 29) and pathophysiological (52, 58) processes. Ezrin is one of the host cytoskeletal proteins reorganized following EPEC infection (17). Here we examine the impact of this important enteric bacterial pathogen on ezrin activation and explore its involvement in EPEC pathogenesis.. In contrast to prototypic enteric bacterial pathogens, EPEC produces no recognized toxin and is essentially noninvasive. Instead, through a series of complex steps, EPEC intimately ...
Citrobacter freundii ATCC ® 8090™ Designation: TypeStrain=True Application: Produces restriction endonuclease CfrAI Quality control strain Reference material Quality control strain for Sensititre products
Citrobacter freundii ATCC ® 8090™ Designation: TypeStrain=True Application: Produces restriction endonuclease CfrAI Quality control strain Reference material Quality control strain for Sensititre products
Simoni, Y., Fehlings, M., Kløverpris, H.N. et al.. Animal models have highlighted the importance of innate lymphoid cells (ILCs) in multiple immune responses. However, technical limitations have hampered adequate characterization of ILCs in humans. Here, we used mass cytometry including a broad range of surface markers and transcription factors to accurately identify and profile ILCs across healthy and inflamed tissue types. High dimensional analysis allowed for clear phenotypic delineation of ILC2 and ILC3 subsets. We were not able to detect ILC1 cells in any of the tissues assessed, however, we identified intra-epithelial (ie)ILC1-like cells that represent a broader category of NK cells in mucosal and non-mucosal pathological tissues. In addition, we have revealed the expression of phenotypic molecules that have not been previously described for ILCs. Our analysis shows that human ILCs are highly heterogeneous cell types between individuals and tissues. It also provides a global, ...
Professor PAN Lei of the Institute of Biophysics (IBP) of the Chinese Academy of Sciences in cooperation with Professor TANG Hong (Institute Pasteur of Shanghai) and colleagues found that flies deficient of intestinal Bap180 (Baf180 in mammals), a subunit of chromatin remodeling SWI/SNF complex, succumb to excessive inflammation rather than bacterial overload after bacterial infection. Bap180 is induced by Drosophila intestinal innate immune pathway, IMD-Relish signalling (TNFR/IL-1R in mammals), response to bacterial challenge. Thus,upregulated Bap180 functions as a negative feedback regulator to limit overreactive IMD signaling through interfering with Relish binding activity as well as to avoid overexpression of pro-inflammatory gene eiger (TNF in mammals), a critical step to prevent of excessive tissue damage and elongate life span of flies, at transcriptional level. Furthermore, intestinal targeting of Baf180 renders mice susceptible to a more aggressive infectious colitis caused by ...
Salmonella and Citrobacter rodentium. Intracellular bacteria trigger activation of the inflammasome, which results in specific ...
... independent inflammatory responses following infection by enteropathogenic Escherichia coli and Citrobacter rodentium". ...
... inhibitor of the bacterial type III secretion system protects against in vivo infection with Citrobacter rodentium". The ...
... coli directly competes with Citrobacter rodentium for carbohydrates in the intestinal lumen) or by producing growth inhibitors ...
... in EPEC endemic areas The serum of EPEC/EHEC infected children and EPEC infected volunteers Secretions of Citrobacter rodentium ...
Citrobacter rodentium Induces Tissue-Resident Memory CD4(+) T Cells. Infect Immun 87, (2019). Wu YM, Cieslik M, Lonigro RJ, et ...
... and they do not survive infection by the intestinal pathogen Citrobacter rodentium. The same authors reported that in wild-type ... that overexpress Cyp1a1 in the gut epithelium led to a pseudo-AHR-deficient state and when infected with Citrobacter rodentium ...
Citrobacter freundii MeSH B03.440.450.425.200.475 - Citrobacter koseri MeSH B03.440.450.425.200.737 - Citrobacter rodentium ... Citrobacter freundii MeSH B03.660.250.150.100.475 - Citrobacter koseri MeSH B03.660.250.150.100.737 - Citrobacter rodentium ...
... such as gastrointestinal Citrobacter rodentium infection. Retinoic acid also enhances the expression of gut- homing markers on ...
"Infection with enteric pathogens Salmonella typhimurium and Citrobacter rodentium modulate TGF-beta/Smad signaling pathways in ...
"Citrobacter rodentium" at the Encyclopedia of Life LPSN Type strain of Citrobacter rodentium at BacDive - the Bacterial ... Citrobacter rodentium is a Gram-negative species of bacteria. Schauer DB, Zabel BA, Pedraza IF, O'Hara CM, Steigerwalt AG, ... Mundy R, MacDonald TT, Dougan G, Frankel G, Wiles S (2005). "Citrobacter rodentium of mice and man". Cell Microbiol. 7 (12): ... Bhinder G, Sham HP, Chan JM, Morampudi V, Jacobson K, Vallance BA (2013). "The Citrobacter rodentium mouse model: studying ...
"Citrobacter rodentium" at the Encyclopedia of Life LPSN Type strain of Citrobacter rodentium at BacDive - the Bacterial ... Citrobacter rodentium is a Gram-negative species of bacteria. Schauer DB, Zabel BA, Pedraza IF, OHara CM, Steigerwalt AG, ... Mundy R, MacDonald TT, Dougan G, Frankel G, Wiles S (2005). "Citrobacter rodentium of mice and man". Cell Microbiol. 7 (12): ... Bhinder G, Sham HP, Chan JM, Morampudi V, Jacobson K, Vallance BA (2013). "The Citrobacter rodentium mouse model: studying ...
Thus, C. rodentium has long been used as a model to … ... Citrobacter rodentium is a mucosal pathogen of mice that shares ... Citrobacter rodentium: infection, inflammation and the microbiota Nat Rev Microbiol. 2014 Sep;12(9):612-23. doi: 10.1038/ ... Citrobacter rodentium is a mucosal pathogen of mice that shares several pathogenic mechanisms with enteropathogenic Escherichia ... Thus, C. rodentium has long been used as a model to understand the molecular basis of EPEC and EHEC infection in vivo. In this ...
Methane metabolism - Citrobacter rodentium [ Pathway menu , Organism menu , Pathway entry , Download KGML , Show description , ...
"Citrobacter rodentium" by people in Harvard Catalyst Profiles by year, and whether "Citrobacter rodentium" was a major or minor ... "Citrobacter rodentium" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... Virulence factors enhance Citrobacter rodentium expansion through aerobic respiration. Science. 2016 09 16; 353(6305):1249-53. ... Below are the most recent publications written about "Citrobacter rodentium" by people in Profiles. ...
Citrobacter rodentium, a mucosal pathogen found in mice, and enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E ... After Citrobacter rodentium infection, the histopathology scores indicated that COS feeding resulted in less severe colitis. IL ... R. Mundy, T. T. MacDonald, G. Dougan, G. Frankel, and S. Wiles, "Citrobacter rodentium of mice and man," Cellular Microbiology ... S. A. Luperchio, J. V. Newman, C. A. Dangler et al., "Citrobacter rodentium, the causative agent of transmissible murine ...
Citrobacter rodentium induced liver changes in C57BL/6 mice : animal model of acute inflammatory stress and injury. Download ... Citrobacter rodentium induced liver changes in C57BL/6 mice : animal model of acute inflammatory stress and injury. Research ... Using Citrobacter rodentium, a well characterized rodent-specific enteric pathogen as a source of extrahepatic inflammatory ... C. rodentium-induced inflammatory stress was finally investigated for its potential in altering drug pharmacokinetics (PK) of ...
Forty-eight mice were randomly assigned to six groups: basal diet (CTRL), intragastric administration Citrobacter rodentium (CR ... Forty-eight mice were randomly assigned to six groups: basal diet (CTRL), intragastric administration Citrobacter rodentium (CR ... to treat enteritis in a mouse model of Citrobacter rodentium-induced colitis by evaluating serum metabolomics and gut microbes ... to treat enteritis in a mouse model of Citrobacter rodentium-induced colitis by evaluating serum metabolomics and gut microbes ...
Citrobacter rodentium is a murine enteropathogen which infects mice using the same modus operandi as EPEC and EHEC, allowing ... Unpacking the Unknown: Characterisation of Citrobacter rodentium extracellular vesicles. ResearchSpace/Manakin Repository. ... As prior studies have shown EV production by E. coli, this begs the question of whether the same is true for C. rodentium, ... My results show that the concentration of EVs produced by C. rodentium in both rich and defined media is low compared to that ...
Citrobacter rodentium, formerly Citrobacter freundii biotype 4280, causes transmissible murine colonic hyperplasia (6, 45, 46 ... Citrobacter rodentium Infection in Mice Elicits a Mucosal Th1 Cytokine Response and Lesions Similar to Those in Murine ... Citrobacter rodentium Infection in Mice Elicits a Mucosal Th1 Cytokine Response and Lesions Similar to Those in Murine ... Citrobacter rodentium Infection in Mice Elicits a Mucosal Th1 Cytokine Response and Lesions Similar to Those in Murine ...
744993-role-of-class-1-serine-protease-autotransporter-in-the-pathogenesis-of-citrobacter-rodentium-colitis. ... Role of Class 1 Serine Protease Autotransporter in the Pathogenesis of Citrobacter rodentium Colitis. ...
The mouse pathogen Citrobacter rodentium encodes one NleH protein, which functions equivalently to E. coli NleH1. We examined ... Influence of NleH effector expression, host genetics, and inflammation on Citrobacter rodentium colonization of mice. en_US. ... Influence of NleH effector expression, host genetics, and inflammation on Citrobacter rodentium colonization of mice. K-REx ... C. rodentium that expressed both E. coli NleH1 and NleH2 was hypervirulent in C3H/HeJ mice.. en_US. ...
In order to colonize the host and compete with the gut microbiota, C. rodentium employs a type III secretion system (T3SS) that ... Importantly, while the reduced CCH and abundance of antimicrobial proteins during ΔespO infection did not affect C. rodentium ... Of the main hallmarks of C. rodentium infection are colonic crypt hyperplasia (CCH) and dysbiosis. ... rodentium infection as well as secretion of IL-22 from colonic explants. While we observed no differences in the recruitment of ...
Intimin-specific immune responses prevent bacterial colonization by the attaching-effacing pathogen Citrobacter rodentium ... Intimin-specific immune responses prevent bacterial colonization by the attaching-effacing pathogen Citrobacter rodentium ...
Crepin, VF; Collins, JW; Habibzay, M; Frankel, G; (2016) Citrobacter rodentium mouse model of bacterial infection. Nature ... Infection of mice with Citrobacter rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health ... C. rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was rediscovered ...
... is-a-global-transcriptional-regulator-that-controls-virulence-gene-expression-in-citrobacter-rodentium. ... Is a Global Transcriptional Regulator That Controls Virulence Gene Expression in Citrobacter rodentium. ... We thank Rosanna Mundy (Imperial College, London, United Kingdom) for constructing the STM library of C. rodentium, Judyta ...
... using the mouse pathogen Citrobacter rodentium (CR). Treatment of mice with FDP formulas A, B, and C or a control product did ... Fermented dairy products modulate Citrobacter rodentium-induced colonic hyperplasia. The Journal of infectious diseases, 210 (7 ...
rodentium infection led to a rapid increase of these cells. There were more S100A4+ cells in the C. rodentium affected colon on ... rodentium-infected mouse colons. It is still not clear whether S100A4 is expressed in the mouse colon during C. rodentium ... Here, upon infection with Citrobacter rodentium, a model for enteropathogenic Escherichia coli infection in humans, induced the ... rodentium in 200 μl PBS. Various tissues were collected both prior to and during C. rodentium infection. The mRNA expression of ...
Gareau, M., Wine, E., Reardon, C., & Sherman, P. M. (2010). Probiotics prevent death caused by Citrobacter rodentium Infection ... Probiotics prevent death caused by Citrobacter rodentium Infection in neonatal mice. Melanie Gareau, Eytan Wine, Colin Reardon ... Gareau, M, Wine, E, Reardon, C & Sherman, PM 2010, Probiotics prevent death caused by Citrobacter rodentium Infection in ... Probiotics prevent death caused by Citrobacter rodentium Infection in neonatal mice. / Gareau, Melanie; Wine, Eytan; Reardon, ...
Osteopontin mediates Citrobacter rodentium-induced colonic epithelial cell hyperplasia and attaching-effacing lesions. / Wine, ... Osteopontin mediates Citrobacter rodentium-induced colonic epithelial cell hyperplasia and attaching-effacing lesions. American ... title = "Osteopontin mediates Citrobacter rodentium-induced colonic epithelial cell hyperplasia and attaching-effacing lesions ... T1 - Osteopontin mediates Citrobacter rodentium-induced colonic epithelial cell hyperplasia and attaching-effacing lesions ...
Citrobacter rodentium subverts ATP flux and cholesterol homeostasis in intestinal epithelial cells in vivo. Cell Metabolism 26 ... Citrobacter rodentium subverts ATP flux and cholesterol homeostasis in intestinal epithelial cells in vivo ... We investigated the impact of infection with the enteric pathogen Citrobacter rodentium on mouse IEC metabolism using global ... These results suggest that C. rodentium manipulates host metabolism to evade innate immune responses and establish a favorable ...
Enhanced susceptibility to Citrobacter rodentium infection in microRNA-155-deficient mice. Simon Clare, Victoria John, Alan W ... Enhanced susceptibility to Citrobacter rodentium infection in microRNA-155-deficient mice. Infection and Immunity. 2013 Mar;81( ... Enhanced susceptibility to Citrobacter rodentium infection in microRNA-155-deficient mice. In: Infection and Immunity. 2013 ; ... Enhanced susceptibility to Citrobacter rodentium infection in microRNA-155-deficient mice. / Clare, Simon; John, Victoria; ...
Fingerprint Dive into the research topics of Streptococcus pneumoniae-induced pneumonia and citrobacter rodentium-induced gut ... T1 - Streptococcus pneumoniae-induced pneumonia and citrobacter rodentium-induced gut infection differentially alter vitamin A ... Streptococcus pneumoniae-induced pneumonia and citrobacter rodentium-induced gut infection differentially alter vitamin A ... Streptococcus pneumoniae-induced pneumonia and citrobacter rodentium-induced gut infection differentially alter vitamin A ...
Salmonella and Citrobacter rodentium. Intracellular bacteria trigger activation of the inflammasome, which results in specific ...
mTOR is critical for intestinal T-cell homeostasis and resistance to Citrobacter rodentium *Xingguang Lin ... Rights & permissionsfor article mTOR is critical for intestinal T-cell homeostasis and resistance to ,i,Citrobacter rodentium,/ ...
CD4+ T cells drive goblet cell depletion during Citrobacter rodentium infection. * Authors: Chan JM, Bhinder G, Sham HP, Ryz N ... Mice lacking CD4+ T cells or B cells are highly susceptible to Citrobacter rodentium infection. In this study, we show that the ... The p50 subunit of NF-kappaB is critical for in vivo clearance of the noninvasive enteric pathogen Citrobacter rodentium. ... Gamma interferon produced by antigen-specific CD4+ T cells regulates the mucosal immune responses to Citrobacter rodentium ...
Citrobacter rodentium. *Mycobacterium bovis - Bacillus Calmette-Guérin (BCG). Parasitic pathogens. *Plasmodium chabaudi (blood ...
Human enterohemorrhagic Escherichia coli (EHEC), enteropathogenic E. coli, and the mouse pathogen Citrobacter rodentium (CR) ... Diarrheagenic enterohemorrhagic Escherichia coli (EHEC), enteropathogenic E. coli (EPEC), and Citrobacter rodentium (CR) are ... Citrobacter rodentium; A/E, attaching/effacing; LEE, locus of enterocyte effacement; TTSS, type III secretion system; TTS, type ... Table 1. Functional characterization of the 41 gene deletion mutants of the locus of enterocyte effacement in C. rodentium ...
C. rodentium-induced colitis is attenuated in ILK-ko mice, and ILK is induced in response to infection. The C. rodentium ... MacDonald TT, Frankel G, Dougan G, Goncalves NS, Simmons C: Host defences to citrobacter rodentium. Int J Med Microbiol. 2003, ... Here we report on the role of epithelial derived ILK in response to Citrobacter rodentium infection. ... Wang Y, Xiang GS, Kourouma F, Umar S: Citrobacter rodentium-induced NF-kappaB activation in hyperproliferating colonic ...
4D Multimodality Imaging of Citrobacter rodentium Infections in Mice, Radionuclide-fluorescence Reporter Gene Imaging to ... 4D Multimodality Imaging of Citrobacter rodentium Infections in Mice. James William Collins1, Jeffrey A Meganck2, Chaincy Kuo2 ...
ECO: Escherichia coli MG1655, CKO: Citrobacter koseri, CRO: Citrobacter rodentium, STM: Salmonella Typhimurium LT2, ENT: ...
  • The mouse pathogen Citrobacter rodentium encodes one NleH protein, which functions equivalently to E. coli NleH1. (k-state.edu)
  • We evaluated the protective effects of fermented dairy products (FDPs) in an infection model, using the mouse pathogen Citrobacter rodentium (CR). (lshtm.ac.uk)
  • The objective of this study was to determine the role of OPN in host responses to a non-invasive bacterial pathogen, Citrobacter rodentium, which serves as a murine infectious model of colitis. (elsevier.com)
  • We investigated the impact of infection with the enteric pathogen Citrobacter rodentium on mouse IEC metabolism using global proteomic and targeted metabolomics and lipidomics. (cf.ac.uk)
  • The p50 subunit of NF-kappaB is critical for in vivo clearance of the noninvasive enteric pathogen Citrobacter rodentium. (helmholtz-hzi.de)
  • Central role for B lymphocytes and CD4+ T cells in immunity to infection by the attaching and effacing pathogen Citrobacter rodentium. (helmholtz-hzi.de)
  • Human enterohemorrhagic Escherichia coli (EHEC), enteropathogenic E. coli , and the mouse pathogen Citrobacter rodentium (CR) possess the locus of enterocyte effacement (LEE) PAI. (pnas.org)
  • To determine if pst contributes to bacterial colonization in vivo, a pstCA mutation was made in the EPEC-like murine pathogen, Citrobacter rodentium. (monash.edu)
  • The team infected mice with the murine pathogen Citrobacter rodentium , which establishes first in the cecum. (mentalfloss.com)
  • In this Review, we discuss recent studies in which C. rodentium has been used to study mucosal immunology, including the deregulation of intestinal inflammatory responses during bacteria-induced colitis and the role of the intestinal microbiota in mediating resistance to colonization by enteric pathogens. (nih.gov)
  • After Citrobacter rodentium infection, the histopathology scores indicated that COS feeding resulted in less severe colitis. (hindawi.com)
  • A number of significant intestinal disorders found in humans are also frequently modelled by C. rodentium in mice, such as colon tumorigenesis, ulcerative colitis, and Crohn's disease [ 5 ]. (hindawi.com)
  • Colitis develops in mice that have been infected with C. rodentium , which results in the bacteria becoming overabundant and the mice's natural microbiota reducing in variety and quantity [ 6 ]. (hindawi.com)
  • The genetic makeup of the mouse impacts the formation of C. rodentium -induced colitis, with mice such as C3H/HeJ and FVB/N being prone to develop colitis as a result of the infection and mice such as CD-1 and C57BL/6 being considered amongst those that are not prone to develop colitis and are only prone to subclinical symptoms [ 9 ]. (hindawi.com)
  • This study aimed to evaluate the abilities of two peptides derived from egg albumin transferrin, IRW and IQW, to treat enteritis in a mouse model of Citrobacter rodentium -induced colitis by evaluating serum metabolomics and gut microbes. (frontiersin.org)
  • Therefore, these data indicate a novel mechanism for S100A4 that promotes colitis development by enhancing host adhesion and colonization of Citrobacter rodentium through the S100A4-mediated host inflammatory responses. (medicalrecords.com)
  • Therefore, infection of mice with C . rodentium is an excellent in vivo model of colitis. (medicalrecords.com)
  • For this purpose, we used S100A4 knock out ( S100A4 −/− ) and wild-type (WT) mice orally challenged with C . rodentium to establish a model for studying the role of S100A4 and its related molecular mechanism in colitis. (medicalrecords.com)
  • Moreover, the pro-resolving properties of KO were validated using a Th1-inducing Citrobacter rodentium colitis murine model. (usda.gov)
  • Here, we show that in vivo depletion of CX 3 CR1 + mononuclear phagocytes (MNPs) resulted in more severe colitis and death after infection with Citrobacter rodentium . (rupress.org)
  • We evaluated the intestinal microbiota, induced colitis with Citrobacter rodentium and followed disease progression. (omega-research.com)
  • During infection-induced colitis, ω-6 PUFA fed mice had exacerbated intestinal damage, immune cell infiltration, prostaglandin E2 expression and C. rodentium translocation across the intestinal mucosae. (omega-research.com)
  • Citrobacter rodentium , a mucosal pathogen found in mice, and enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E. coli (EHEC), enteric pathogens found in humans, create attaching and effacing (A/E) lesions that result in the colonization of mucosa within the intestinal tract [ 1 , 2 ]. (hindawi.com)
  • None of the changes were seen in mice inoculated with bacteria lacking intimin (which is necessary for colonization), but they were seen in mice inoculated with C. rodentium complemented with intimin from EPEC. (asm.org)
  • We examined the impact of host genetics and intestinal inflammation on the contribution of NleH to C. rodentium colonization of mice differing in LPS responsiveness. (k-state.edu)
  • Importantly, while the reduced CCH and abundance of antimicrobial proteins during ΔespO infection did not affect C. rodentium colonization or the composition of commensal Proteobacteria, they had a subtle consequence on Firmicutes subpopulations. (inserm.fr)
  • Therefore, lack of OPN results in decreased pedestal formation, colonization, and colonic epithelial cell hyperplasia responses to C. rodentium infection, indicating that OPN impacts disease pathogenesis through bacterial attachment and altered host immune responses. (elsevier.com)
  • miR-155-deficient mice exhibited prolonged colonization associated with a higher C. rodentium burden in gastrointestinal tissue and spread into systemic tissues. (elsevier.com)
  • This was not due to reduced colonization, but was associated with an altered pattern of C. rodentium bacterial migration. (biomedcentral.com)
  • ILK influences the host response to C. rodentium -induced infection, independently of reduced colonization in the ILK knockout mice. (biomedcentral.com)
  • Identification of a novel type IV pilus gene cluster required for gastrointestinal colonization of Citrobacter rodentium. (ox.ac.uk)
  • In order to identify genes required for the colonization of A/E-forming pathogens, a library of signature-tagged transposon mutants of C. rodentium was constructed and screened in mice. (ox.ac.uk)
  • The region flanking the transposon insertion was sequenced, identifying a cluster of 12 genes that encode the first described pilus of C. rodentium (named colonization factor Citrobacter, CFC). (ox.ac.uk)
  • A non-polar mutation in cfcI, complementation of this strain with wild-type cfcI and complementation of strain P5H2 with wild-type cfcH confirmed that these genes are required for colonization of the gastrointestinal tract by C. rodentium. (ox.ac.uk)
  • This loss of tolerance in monocytes results in greater colonization resistance towards Citrobacter rodentium. (uni-koeln.de)
  • Citrobacter rodentium is a mucosal pathogen of mice that shares several pathogenic mechanisms with enteropathogenic Escherichia coli (EPEC) and enterohaemorrhagic E. coli (EHEC), which are two clinically important human gastrointestinal pathogens. (nih.gov)
  • Citrobacter rodentium is a classically noninvasive pathogen of mice that is similar to enteropathogenic Escherichia coli (EPEC) in man. (asm.org)
  • Here, upon infection with Citrobacter rodentium , a model for enteropathogenic Escherichia coli infection in humans, induced the infiltration of a large number of S100A4 + cells into the colon in wild type (WT) mice. (medicalrecords.com)
  • Diarrheagenic enterohemorrhagic Escherichia coli (EHEC), enteropathogenic E. coli (EPEC), and Citrobacter rodentium (CR) are attaching/effacing (A/E) bacterial pathogens that attach to host intestinal epithelium and efface brush border microvilli, forming A/E lesions ( 1 , 2 ). (pnas.org)
  • Citrobacter rodentium is used as an in vivo model system for clinically significant enteric pathogens such as enterohaemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC). (ox.ac.uk)
  • Intestinal epithelial barrier damage was assessed in Caco-2 cells incubated with three important enteropathogens identified in EE patients: Enteropathogenic Escherichia coli (EPEC), Citrobacter rodentium ( C. rodentium ), and Cryptosporidium parvum ( C. parvum ). (springer.com)
  • RT "The Citrobacter rodentium genome sequence reveals convergent RT evolution with human pathogenic Escherichia coli. (genome.jp)
  • Modulation of host cytoskeleton function by the enteropathogenic Escherichia coli and Citrobacter rodentium effector protein EspG. (k-state.edu)
  • The NF-κB transcription factor c-Rel controls host defense against Citrobacter rodentium. (helmholtz-hzi.de)
  • When infected, 1-3% of the mice's intestinal microbiota becomes C. rodentium [ 7 ], whilst the colon comes under attack by 10 9 colony forming units (CFUs) per g [ 8 ]. (hindawi.com)
  • Vulnerability to contracting C. rodentium , as well as tendency to show a certain immune response, has been found to be highly related to intestinal microbiota composition [ 10 ]. (hindawi.com)
  • In order to colonize the host and compete with the gut microbiota, C. rodentium employs a type III secretion system (T3SS) that injects effectors into colonic intestinal epithelial cells (IECs). (inserm.fr)
  • Infection of mice with Citrobacter rodentium is a robust model to study bacterial pathogenesis, mucosal immunology, the health benefits of probiotics and the role of the microbiota during infection. (lshtm.ac.uk)
  • In conclusion, gastrointestinal infection with C. rodentium alters systemic and hepatocytes specific responses, not previously appreciated from this enteric pathogen, making it a useful model for studying host-pathogen interactions under acute hepatic inflammatory stress and injury. (mit.edu)
  • Complete Genome Sequence of Citrobacter rodentium Strain DBS100. (nih.gov)
  • C57BL/6 mice were tested in order to investigate the effects of dietary chitosan (COS) supplements on intestinal microflora and resistance to Citrobacter rodentium infection. (hindawi.com)
  • NleH expression was detrimental to C. rodentium in C57BL/10ScNJ mice, which do not mount LPS-induced inflammatory responses. (k-state.edu)
  • Infection of C57BL/6 mice with C. rodentium was performed at postnatal day 14. (elsevier.com)
  • Here, we show that miR-155-deficient mice are less able to eradicate a mucosal Citrobacter rodentium infection than wild-type C57BL/6 mice. (elsevier.com)
  • C57BL/6 mice infected perorally with the pstCA mutant of C. rodentium excreted significantly lower numbers of C. rodentium than those given the wild-type strain. (monash.edu)
  • Enteropathogenic E. coli (EPEC), Enterohaemorhagic E. coli (EHEC) and Citrobacter rodentium are constituent members of the attaching and effacing (A/E) pathogens. (bl.uk)
  • My results show that the concentration of EVs produced by C. rodentium in both rich and defined media is low compared to that reported for other bacterial species. (auckland.ac.nz)
  • Citrobacter rodentium mouse model of bacterial infection. (lshtm.ac.uk)
  • Indole-3-carbinol inhibits Citrobacter rodentium infection through multiple pathways including reduction of bacterial adhesion and enhancement of cytotoxic T cell activity. (usda.gov)
  • Since T-cell responses in mouse models of inflammatory bowel disease (IBD) also cause epithelial hyperplasia, we have investigated the possibility that C. rodentium promotes similar T-cell responses in the mucosa, thereby increasing epithelial shedding, transmission, and replication of the organism. (asm.org)
  • Citrobacter rodentium , formerly Citrobacter freundii biotype 4280, causes transmissible murine colonic hyperplasia ( 6 , 45 , 46 ). (asm.org)
  • Of the main hallmarks of C. rodentium infection are colonic crypt hyperplasia (CCH) and dysbiosis. (inserm.fr)
  • Fermented dairy products modulate Citrobacter rodentium-induced colonic hyperplasia. (lshtm.ac.uk)
  • Weight loss, colonic epithelial cell hyperplasia, mucosal barrier dysfunction, and elevated serum corticosterone levels in C. rodentium-infected wild-type mice were ameliorated by probiotics, but not in ragl -/- animals. (elsevier.com)
  • Furthermore, colonic epithelial cell hyperplasia, the hallmark of C. rodentium infection, was reduced in OPN -/- mice, and spleen enlargement by infection was absent in OPN -/- mice. (elsevier.com)
  • Sherman, Philip M. / Osteopontin mediates Citrobacter rodentium-induced colonic epithelial cell hyperplasia and attaching-effacing lesions . (elsevier.com)
  • Moreover, colonic hyperplasia and diarrhea, which are features of infections with C. rodentium, were not observed in mice infected with the pstCA mutant but did occur in mice given the trans-complemented mutant. (monash.edu)
  • Citrobacter rodentium (CR) promotes crypt hyperplasia and tumorigenesis by aberrantly regulating Wnt/β-catenin signaling. (sigmaaldrich.com)
  • Thus, C. rodentium has long been used as a model to understand the molecular basis of EPEC and EHEC infection in vivo. (nih.gov)
  • C. rodentium amongst mice populations has been used by many researchers to represent intestinal E. coli since intestinal EPEC or EHEC does not infect mice. (hindawi.com)
  • Citrobacter rodentium is a murine enteropathogen which infects mice using the same 'modus operandi' as EPEC and EHEC, allowing many aspects of pathogenesis to be explored in vivo. (auckland.ac.nz)
  • The work I present in this thesis lays the foundations for future studies of the role of EVs in vivo, using infection of mice by C. rodentium as a convenient model system for EPEC and EHEC. (auckland.ac.nz)
  • Both EPEC and EHEC are poorly pathogenic in mice, but C . rodentium is a Gram-negative A/E bacterium that specifically infects the mouse colon epithelial cells and causes damage to the epithelial layer 10 , 11 . (medicalrecords.com)
  • The group observed a similar pattern when mice were infected with their equivalent of EHEC, the gut bacterium Citrobacter rodentium. (utsouthwestern.edu)
  • C. rodentium is used in mice to mimic the effects EHEC produces in humans. (liberty.edu)
  • Citrobacter rodentium is a murine pathogen which is an excellent animal model for EPEC and EHEC infection. (bl.uk)
  • EPEC, EHEC and C. rodentium conserve a genomic region termed the locus of enterocyte effacement (LEE) which encodes a type 3 secretion system (T3SS), a core set of type 3 secreted effector proteins and the outer membrane adhesin intimin, which are essential for A/E lesion formation. (bl.uk)
  • In vitro , soluble S100A4 directly up-regulated expression of integrin β−1 in intestinal epithelial cells and significantly increased the adherence of C . rodentium to intestinal epithelial cells. (medicalrecords.com)
  • Additionally, the effects of S100A4 on the adherence of C . rodentium to epithelial cells could be abolished by a receptor for advanced glycation end products (RAGE)-specific inhibitor (FPS-ZM1). (medicalrecords.com)
  • Here we report on the role of epithelial derived ILK in response to Citrobacter rodentium infection. (biomedcentral.com)
  • C. rodentium was administered to both control and intestinal epithelial cell ILK knockout mice. (biomedcentral.com)
  • Active vitamin D (1,25-dihydroxyvitamin D3) increases host susceptibility to Citrobacter rodentium by suppressing mucosal Th17 responses. (greenmedinfo.com)
  • and these changes led to better control of inflammation and resolution of infection with C. rodentium . (hindawi.com)
  • OS Citrobacter rodentium (strain ICC168) (Citrobacter freundii biotype OS 4280). (genome.jp)
  • To better understand how lung and gastrointestinal pathogens affect VA status, we assessed VA concentrations in serum, lung, and liver during an invasive pneumonia infection induced by Streptococcus pneumoniae serotype 3, and a noninvasive gut infection induced by Citrobacter rodentium, in vitamin A-adequate (VAA) and vitamin A-deficient (VAD) mice. (elsevier.com)
  • Though the Citrobacter rodentium ( C. rodentium ) strain DBS100 has been studied extensively, it had not previously been sequenced. (liberty.edu)
  • Next, the investigators tried the same experiment using Citrobacter rodentium - a strain of bacteria similar to the E. coli strains that affect humans. (medicalnewstoday.com)
  • Citrobacter rodentium is a Gram-negative species of bacteria. (wikipedia.org)
  • They infected the mice with Citrobacter rodentium, a species of bacteria that is the rodent equivalent of E. coli, which infects humans. (eurekalert.org)
  • pathogens with the closely related human pathogen, en- teropathogenic E. coli ( 4 , 5 ). (cdc.gov)
  • Therefore, the aims of this study were to characterize Citrobacter rodentium infection in neonatal mice and determine the role played by specific probiotics in ameliorating disease severity. (elsevier.com)
  • Probiotic Lactobacillus reuteri attenuates the stressor-enhanced severity of Citrobacter rodentium infection. (greenmedinfo.com)
  • Infection with Citrobacter rodentium triggers robust tissue damage repair responses, manifested by secretion of IL-22, in the absence of which mice succumbed to the infection. (inserm.fr)
  • These results suggest that C. rodentium manipulates host metabolism to evade innate immune responses and establish a favorable gut ecosystem. (cf.ac.uk)
  • Germinal center formation and humoral immune responses against C. rodentium were severely impaired in infected miR-155-deficient mice. (elsevier.com)
  • Gamma interferon produced by antigen-specific CD4+ T cells regulates the mucosal immune responses to Citrobacter rodentium infection. (helmholtz-hzi.de)
  • Here we report that the effector EspO ,an orthologue of OspE found in Shigella spp, affects proliferation of IECs 8 and 14 days post C. rodentium infection as well as secretion of IL-22 from colonic explants. (inserm.fr)
  • However, since Moxley and Francis's review in 1998 ( 2 ), several advances have been made in the field, including the generation of a Shiga toxin (Stx)-producing Citrobacter rodentium -murine model, a human intestine xenograft murine model, and a renewed interest in the use of rabbit models. (asmscience.org)
  • As prior studies have shown EV production by E. coli, this begs the question of whether the same is true for C. rodentium, which would provide a useful model for exploring the role of EVs in pathogenicity. (auckland.ac.nz)
  • Pomegranate peel extract reduced the pathogenicity of Citrobacter rodentium-infections in mice. (usda.gov)
  • In our previous study, Citrobacter werkmanii BF-6 was isolated from an industrial spoilage sample and demonstrated an excellent ability to form biofilms, which could be affected by various environmental factors. (biomedcentral.com)
  • C. rodentium that expressed both E. coli NleH1 and NleH2 was hypervirulent in C3H/HeJ mice. (k-state.edu)
  • Consequently, these mice are susceptible to C. rodentium infection, and both exogenous IL-22 and IL-23 are able to restore the mucosal host defence. (nih.gov)
  • While we observed no differences in the recruitment of group 3 innate lymphoid cells (ILC3s) and T cells, which are the main sources of IL-22 at the early and late stages of C. rodentium infection respectively, infection with ΔespO was characterized by diminished recruitment of sub-mucosal neutrophils, which coincided with lower abundance of Mmp9 and chemokines (e.g. (inserm.fr)
  • We find that the induction of IL-22 from innate lymphoid cells and CD4(+) T cells is impaired in obese mice under various immune challenges, especially in the colon during infection with Citrobacter rodentium. (nih.gov)
  • To investigate this, we inactivated phoB in the pstCA mutants of EPEC E128012 and C. rodentium and found that the phoB mutation restored the adherent phenotype of both mutant strains. (monash.edu)
  • Moreover, mice infected with ΔespO triggered significantly lesser nutritional immunity (e.g. calprotectin, Lcn2) and expression of antimicrobial peptides (Reg3β, Reg3γ) compared to mice infected with WT C. rodentium. (inserm.fr)
  • Critical role of T cell-dependent serum antibody, but not the gut-associated lymphoid tissue, for surviving acute mucosal infection with Citrobacter rodentium, an attaching and effacing pathogen. (helmholtz-hzi.de)
  • Pomegranate peel extract alters the microbiome in mice and dysbiosis caused by Citrobacter rodentium infection. (usda.gov)
  • Dietary oils modify the host immune response and colonic tissue damage following Citrobacter rodentium infection in mice. (greenmedinfo.com)
  • C. rodentium was first isolated by Barthold from an outbreak of mouse diarrhea in Yale University in 1972 and was 'rediscovered' by Falkow and Schauer in 1993. (lshtm.ac.uk)
  • We thank Rosanna Mundy (Imperial College, London, United Kingdom) for constructing the STM library of C. rodentium, Judyta Praszkier (The University of Melbourne) for the gift of plasmids used in this study, Sau Fung Lee (University of Melbourne) for FAS data, and Danijela Krmek for assisting with mouse experiments.This work was supported by grants from the Australian National Health and Medical Research Council and the Australian Research Council. (edu.au)
  • Mouse-derived OPN +/+ and OPN -/- fibroblasts were incubated with C. rodentium and attachingeffacing lesions were demonstrated using transmission electron microscopy and immunofluorescence. (elsevier.com)
  • I observed that there were differences between the protein profiles of C. rodentium grown in rich and defined media, suggesting a change in protein expression or packaging in response to nutrient availability. (auckland.ac.nz)
  • Mice lacking CD4+ T cells or B cells are highly susceptible to Citrobacter rodentium infection. (helmholtz-hzi.de)
  • OPN gene knockout and wild-type mice were infected orogastrically with either C. rodentium or Luria-Bertani (LB) broth. (elsevier.com)
  • Colonic expression of OPN was increased by C. rodentium infection of wild-type mice. (elsevier.com)
  • I did not oberve any differences in the concentration or composition of EVs between the two C. rodentium strains I studied. (auckland.ac.nz)