Reproductive Tract Infections
Genital Diseases, Female
Female Urogenital Diseases
United States Department of Agriculture
CADD, a Chlamydia protein that interacts with death receptors. (1/134)We report here the identification of a bacterial protein capable of interacting with mammalian death receptors in vitro and in vivo. The protein is encoded in the genome of Chlamydia trachomatis and has homologues in other Chlamydia species. This protein, which we refer to as "Chlamydia protein associating with death domains" (CADD), induces apoptosis in a variety of mammalian cell lines when expressed by transient gene transfection. Apoptosis induction can be blocked by Caspase inhibitors, indicating that CADD triggers cell death by engaging the host apoptotic machinery. CADD interacts with death domains of tumor necrosis factor (TNF) family receptors TNFR1, Fas, DR4, and DR5 but not with the respective downstream adaptors. In infected epithelial cells, CADD is expressed late in the infectious cycle of C. trachomatis and co-localizes with Fas in the proximity of the inclusion body. The results suggest a role for CADD modulating the apoptosis pathways of cells infected, revealing a new mechanism of host-pathogen interaction. (+info)
Dynamic diversity of the tryptophan pathway in chlamydiae: reductive evolution and a novel operon for tryptophan recapture. (2/134)BACKGROUND: Complete genomic sequences of closely related organisms, such as the chlamydiae, afford the opportunity to assess significant strain differences against a background of many shared characteristics. The chlamydiae are ubiquitous intracellular parasites that are important pathogens of humans and other organisms. Tryptophan limitation caused by production of interferon-gamma by the host and subsequent induction of indoleamine dioxygenase is a key aspect of the host-parasite interaction. It appears that the chlamydiae have learned to recognize tryptophan depletion as a signal for developmental remodeling. The consequent non-cultivable state of persistence can be increasingly equated to chronic disease conditions. RESULTS: The genes encoding enzymes of tryptophan biosynthesis were the focal point of this study. Chlamydophila psittaci was found to possess a compact operon containing PRPP synthase, kynureninase, and genes encoding all but the first step of tryptophan biosynthesis. All but one of the genes exhibited translational coupling. Other chlamydiae (Chlamydia trachomatis, C. muridarum and Chlamydophila pneumoniae) lack genes encoding PRPP synthase, kynureninase, and either lack tryptophan-pathway genes altogether or exhibit various stages of reductive loss. The origin of the genes comprising the trp operon does not seem to have been from lateral gene transfer. CONCLUSIONS: The factors that accommodate the transition of different chlamydial species to the persistent (chronic) state of pathogenesis include marked differences in strategies deployed to obtain tryptophan from host resources. C. psittaci appears to have a novel mechanism for intercepting an early intermediate of tryptophan catabolism and recycling it back to tryptophan. In effect, a host-parasite metabolic mosaic has evolved for tryptophan recycling. (+info)
Role of proapoptotic BAX in propagation of Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis) and the host inflammatory response. (3/134)The BCL-2 family member BAX plays a critical role in regulating apoptosis. Surprisingly, bax-deficient mice display limited phenotypic abnormalities. Here we investigate the effect of BAX on infection by the sexually transmitted pathogen, Chlamydia muridarum (the mouse pneumonitis strain of Chlamydia trachomatis). Bax(-/-) cells are relatively resistant to Chlamydia-induced apoptosis, and fewer bacteria are recovered after two infection cycles from Bax(-/-) cells than from wild-type cells. These results suggest that BAX-dependent apoptosis may be used to initiate a new round of infection, most likely by releasing Chlamydia-containing apoptotic bodies from infected cells that could be internalized by neighboring uninfected cells. Nonetheless, infected Bax(-/-) cells die through necrosis, which is normally associated with inflammation, more often than infected wild-type cells. These studies were confirmed in mice infected intravaginally with C. muridarum; since the infection disappears more quickly from Bax(-/-) mice than from wild-type mice, secretion of proinflammatory cytokines is increased in Bax(-/-) mice, and large granulomas are present in the genital tract of Bax(-/-) mice. Taken together, these data suggest that chlamydia-induced apoptosis via BAX contributes to bacterial propagation and decreases inflammation. Bax deficiency results in lower infection and an increased inflammatory cytokine response associated with more severe pathology. (+info)
Rab GTPases are recruited to chlamydial inclusions in both a species-dependent and species-independent manner. (4/134)Chlamydiae are obligate intracellular bacteria that replicate within an inclusion that is trafficked to the peri-Golgi region where it fuses with exocytic vesicles. The host and chlamydial proteins that regulate the trafficking of the inclusion have not been identified. Since Rab GTPases are key regulators of membrane trafficking, we examined the intracellular localization of several green fluorescent protein (GFP)-tagged Rab GTPases in chlamydia-infected HeLa cells. GFP-Rab4 and GFP-Rab11, which function in receptor recycling, and GFP-Rab1, which functions in endoplasmic reticulum (ER)-to-Golgi trafficking, are recruited to Chlamydia trachomatis, Chlamydia muridarum, and Chlamydia pneumoniae inclusions, whereas GFP-Rab5, GFP-Rab7, and GFP-Rab9, markers of early and late endosomes, are not. In contrast, GFP-Rab6, which functions in Golgi-to-ER and endosome-to-Golgi trafficking, is associated with C. trachomatis inclusions but not with C. pneumoniae or C. muridarum inclusions, while the opposite was observed for the Golgi-localized GFP-Rab10. Colocalization studies between transferrin and GFP-Rab11 demonstrate that a portion of GFP-Rab11 that localizes to inclusions does not colocalize with transferrin, which suggests that GFP-Rab11's association with the inclusion is not mediated solely through Rab11's association with transferrin-containing recycling endosomes. Finally, GFP-Rab GTPases remain associated with the inclusion even after disassembly of microtubules, which disperses recycling endosomes and the Golgi apparatus within the cytoplasm, suggesting a specific interaction with the inclusion membrane. Consistent with this, GFP-Rab11 colocalizes with C. trachomatis IncG at the inclusion membrane. Therefore, chlamydiae recruit key regulators of membrane trafficking to the inclusion, which may function to regulate the trafficking or fusogenic properties of the inclusion. (+info)
Murine oviduct epithelial cell cytokine responses to Chlamydia muridarum infection include interleukin-12-p70 secretion. (5/134)Epithelial cells play an important role in host defense as sentinels for invading microbial pathogens. Chlamydia trachomatis is an intracellular bacterial pathogen that replicates in reproductive tract epithelium. Epithelial cells lining the reproductive tract likely play a key role in triggering inflammation and adaptive immunity during Chlamydia infections. For this report a murine oviduct epithelial cell line was derived in order to determine how epithelial cells influence innate and adaptive immune responses during Chlamydia infections. As expected, oviduct epithelial cells infected by Chlamydia muridarum produced a broad spectrum of chemokines, including CXCL16, and regulators of the acute-phase response, including interleukin-1alpha (IL-1alpha), IL-6, and tumor necrosis factor alpha. In addition, infected epithelial cells expressed cytokines that augment gamma interferon (IFN) production, including IFN-alpha/beta and IL-12-p70. To my knowledge this is the first report of a non-myeloid/lymphoid cell type making IL-12-p70 in response to an infection. Equally interesting, infected epithelial cells significantly upregulated transforming growth factor alpha precursor expression, suggesting a mechanism by which they might play a direct role in the pathological scarring seen as a consequence of Chlamydia infections. Data from these in vitro studies predict that infected oviduct epithelium contributes significantly to host innate and adaptive defenses but may also participate in the immunopathology seen with Chlamydia infections. (+info)
The infecting dose of Chlamydia muridarum modulates the innate immune response and ascending infection. (6/134)Murine vaginal infection with the obligate intracellular bacterium Chlamydia muridarum is commonly used as a model for ascending Chlamydia infections of the human female genital tract. Gamma interferon-producing Th1 cells, in concert with other mononuclear infiltrates, primarily mediate antichlamydial immunity. However, many factors modify this response, including the bacterial load. To investigate the manner in which the inoculating dose of C. muridarum modulates a genital infection, we measured innate and adaptive cell numbers, CD4+ lymphocyte cytokine profile, chemokine expression, course of infection, and pathological sequelae in genital tracts of BALB/c mice infected with doses of C. muridarum ranging from 10(4) to 10(7) inclusion-forming units. We found that the influx of both innate and adaptive immune cells responded similarly in the lower genital tract (cervical-vaginal tissues) and upper genital tract (oviduct tissues) to increasing inoculating doses. However, cells expressing the innate markers Gr-1 and CD11c were affected to a greater degree by increasing dose than lymphocytes of the adaptive immune response (Th1, CD4+, CD8+, CD19+), resulting in a change in the balance of innate and adaptive cell numbers to favor innate cells at higher infecting doses. Surprisingly, we detected greater numbers of viable chlamydiae in the oviducts at lower inoculating doses, and the number of organisms appeared to directly correlate with hydrosalpinx formation after both primary infection and repeat infection. Taken together, these data suggest that innate immune cells contribute to control of ascending infection. (+info)
Differences in growth characteristics and elementary body associated cytotoxicity between Chlamydia trachomatis oculogenital serovars D and H and Chlamydia muridarum. (7/134)AIM: In vitro growth and elementary body (EB) associated cytotoxicity of two Chlamydia trachomatis strains belonging to serovars D and H and C muridarum were compared to identify difference(s) that correlate with virulence variations between these strains in the mouse model of human female genital tract infection, and phenotypic characteristics that could explain human epidemiological data on serovar prevalence and levels of shedding during serovar D and H infection. METHODS: Replication cycle kinetics, inclusion characteristics, and EB associated cytotoxicity were assessed in McCoy cell monolayers using culture, light microscopy, and lactate dehydrogenase release. RESULTS: Over 72 hours, more rapid production and release of inclusion forming units (ifu) allowed C muridarum to initiate two replication rounds, resulting in 4-8 times more ifu/input unit of infection than with serovars D and H. Although C muridarum EBs were significantly more cytotoxic to McCoy cell monolayers than serovar D at moderate and high multiplicity of infection ratios (MOI), serovar H EBs were significantly more cytotoxic than C muridarum, even at the lowest MOI tested. CONCLUSIONS: These phenotypic differences are consistent with the more invasive course and severe pathological outcome of infection in mice infected with C muridarum, providing an objective basis for questioning the appropriateness of C muridarum as a surrogate for the human biovar of C trachomatis in the murine model of female genital tract infection. The differences seen between the human strains could help explain human epidemiological data relating to differences in prevalence and level of shedding that occurs during infection with oculogenital serovars D and H. (+info)
Molecular basis for the potency of IL-10-deficient dendritic cells as a highly efficient APC system for activating Th1 response. (8/134)Identification and targeting of novel immunobiological factors that regulate the induction of Th1 cells are crucial for designing effective vaccines against certain intracellular pathogens, including Chlamydia. IL-10-deficient dendritic cells (DC) are potent APCs and effective cellular vaccines that activate a high frequency of specific Th1 cells. To elucidate the molecular basis for the potency of the IL-10-deficient APC system, we tested the hypothesis that Chlamydia Ag-primed IL-10 knockout (IL-10KO) DC are quantitatively and qualitatively distinct in their metabolic characteristics relating to T cell activation. Using a combination of RT-PCR, two-dimensional gel electrophoresis, and MALDI-TOF-based proteomics analyses, the transcriptional and translational activities of Chlamydia-pulsed DC from wild-type and IL-10KO mice were assessed. IL-10 deficiency caused early maturation and activation of pulsed DC (i.e., high CD11c, CD40, CD80, CD83, CD86, IL-1, IL-12, and the T cell-attracting chemokine CCL27/CTACK) and consequently an enhanced ability to process and present Ags for a rapid and robust T cell activation. Supporting comparative proteomics revealed further that IL-10 deficient DC possess specific immunobiological properties, e.g., the T cell-attracting chemokine CCL27/CTACK, calcium-dependent protein kinase, and the IL-1/IL-12 inducer, NKR-P1A (CD161), which differentiated them immunologically from wild-type DC that express molecules relating to anti-inflammatory, differentiative, and metabolic processes, e.g., the anti-IL-12 molecule peroxisome proliferator-activated receptor-alpha and thymidine kinase. Collectively, these results provide a molecular basis for the high Th1-activating capacity of IL-10KO APC and may provide unique immunomodulation targets when designing vaccines against pathogens controlled by T cell immunity. (+info)
The symptoms of chlamydia infections can vary depending on the location of the infection. In genital infections, symptoms may include:
* Discharge from the penis or vagina
* Painful urination
* Abnormal bleeding or spotting
* Painful sex
* Testicular pain in men
* Pelvic pain in women
In eye infections, symptoms can include:
* Redness and swelling of the eye
* Discharge from the eye
* Pain or sensitivity to light
In respiratory infections, symptoms may include:
* Shortness of breath or wheezing
If left untreated, chlamydia infections can lead to serious complications, such as pelvic inflammatory disease (PID) in women and epididymitis in men. Chlamydia infections can also increase the risk of infertility and other long-term health problems.
Chlamydia infections are typically diagnosed through a physical examination, medical history, and laboratory tests such as a nucleic acid amplification test (NAAT) or a culture test. Treatment for chlamydia infections typically involves antibiotics, which can effectively cure the infection. It is important to note that sexual partners of someone with a chlamydia infection should also be tested and treated, as they may also have the infection.
Prevention methods for chlamydia infections include safe sex practices such as using condoms and dental dams, as well as regular screening and testing for the infection. It is important to note that chlamydia infections can be asymptomatic, so regular testing is crucial for early detection and treatment.
In conclusion, chlamydia is a common sexually transmitted bacterial infection that can cause serious complications if left untreated. Early detection and treatment are key to preventing long-term health problems and the spread of the infection. Safe sex practices and regular screening are also important for preventing chlamydia infections.
The most common types of RTIs include:
1. Bacterial vaginosis (BV): A condition caused by an imbalance of bacteria in the vagina, which can lead to symptoms such as itching, burning, and discharge.
2. Yeast infections: Caused by a type of fungus called Candida, these infections can cause itching, burning, and discharge.
3. Trichomoniasis: A parasitic infection that can cause itching, burning, and discharge.
4. Chlamydia: A bacterial infection that can cause symptoms such as pain during sex, abnormal bleeding, and difficulty getting pregnant.
5. Gonorrhea: Another bacterial infection that can cause symptoms such as pain during sex, abnormal bleeding, and difficulty getting pregnant.
6. Pelvic inflammatory disease (PID): A type of infection that can cause symptoms such as pelvic pain, fever, and abdominal pain.
RTIs are usually caused by bacteria or viruses, and can be spread through sexual contact or other forms of contact with an infected person. Risk factors for RTIs include having multiple sexual partners, poor hygiene, and using certain types of birth control.
Preventing RTIs includes practicing safe sex, such as using condoms and dental dams, and getting regular check-ups and screenings with a healthcare provider. Treatment for RTIs usually involves antibiotics or other medications, and can help relieve symptoms and prevent long-term complications.
1. Vaginitis: An inflammation of the vagina, often caused by bacterial or yeast infections.
2. Cervicitis: Inflammation of the cervix, often caused by bacterial or viral infections.
3. Endometritis: Inflammation of the lining of the uterus, often caused by bacterial or fungal infections.
4. Pelvic inflammatory disease (PID): A serious infection of the reproductive organs that can cause chronic pelvic pain and infertility.
5. Vulvodynia: Chronic pain of the vulva, often caused by a combination of physical and psychological factors.
6. Vaginal cancer: A rare type of cancer that affects the vagina.
7. Cervical dysplasia: Abnormal cell growth on the cervix, which can develop into cervical cancer if left untreated.
8. Ovarian cysts: Fluid-filled sacs on the ovaries that can cause pelvic pain and other symptoms.
9. Fibroids: Noncancerous growths in the uterus that can cause heavy bleeding, pain, and infertility.
10. Polycystic ovary syndrome (PCOS): A hormonal disorder that can cause irregular menstrual cycles, cysts on the ovaries, and excess hair growth.
These are just a few examples of the many genital diseases that can affect women. It's important for women to practice good hygiene, get regular gynecological check-ups, and seek medical attention if they experience any unusual symptoms to prevent and treat these conditions effectively.
1. Urinary Tract Infections (UTIs): These are infections that occur in the bladder, kidneys, or urethra, and can cause symptoms such as burning during urination, frequent urination, and abdominal pain.
2. Overactive Bladder (OAB): This condition is characterized by sudden, intense urges to urinate, often with urgency and frequency.
3. Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS): This chronic condition causes pain and discomfort in the bladder and pelvic area, and can lead to increased urination and frequency.
4. Vaginal Infections: These are infections that occur in the vagina and can cause symptoms such as itching, burning, and abnormal discharge.
5. Vulvodynia: This chronic condition is characterized by pain and discomfort in the vulva, and can be caused by a range of factors including infection, inflammation, or nerve damage.
6. Endometriosis: This is a condition in which tissue similar to the lining of the uterus grows outside the uterus, causing symptoms such as pelvic pain, heavy menstrual bleeding, and infertility.
7. Polycystic Ovary Syndrome (PCOS): This is a hormonal disorder that can cause symptoms such as irregular menstrual periods, cysts on the ovaries, and excess hair growth.
8. Vaginal Prolapse: This occurs when the muscles and tissues in the vagina weaken, causing the vagina to protrude into the vulva or rectum.
9. Menorrhagia: This is a condition characterized by heavy, prolonged menstrual periods that can cause anemia and other complications.
10. Dyspareunia: This is pain during sexual activity, which can be caused by a range of factors including vaginal dryness, cervical narrowing, or nerve damage.
These are just a few examples of the many conditions that can affect the vulva and vagina. It's important to note that many of these conditions can have similar symptoms, so it's important to see a healthcare provider for an accurate diagnosis and appropriate treatment.
Some common types of vaginal diseases include:
1. Vaginitis: This is an inflammation of the vagina, often caused by bacterial or yeast infections. Symptoms can include itching, burning, and discharge.
2. Bacterial vaginosis (BV): This is a condition caused by an imbalance of bacteria in the vagina, which can lead to symptoms such as itching, burning, and a strong fishy odor.
3. Yeast infection: This is a common condition caused by the overgrowth of candida yeast in the vagina, which can cause symptoms such as itching, burning, and thick, white discharge.
4. Trichomoniasis: This is a sexually transmitted infection (STI) caused by a parasite called Trichomonas vaginalis, which can cause symptoms such as itching, burning, and a thick, yellowish discharge.
5. Vulvodynia: This is a chronic pain condition that affects the vulva (the external female genital area), which can cause symptoms such as pain during sex, itching, and burning.
6. Lichen sclerosus: This is a skin condition that affects the vulva and vagina, which can cause symptoms such as itching, burning, and thickening of the skin.
7. Vulvar cancer: This is a rare type of cancer that affects the vulva, which can cause symptoms such as itching, bleeding, and a lump or sore on the vulva.
Treatment for vaginal diseases depends on the underlying cause and can range from antibiotics and antifungal medications to surgery and lifestyle changes. It's important to seek medical attention if you experience any persistent or severe symptoms, as early diagnosis and treatment can help prevent complications and improve outcomes.
The most common bacteria that cause pneumonia are Streptococcus pneumoniae (also known as pneumococcus), Haemophilus influenzae, and Staphylococcus aureus. These bacteria can infect the lungs through various routes, including respiratory droplets, contaminated food or water, or direct contact with an infected person.
Symptoms of pneumonia may include cough, fever, chills, shortness of breath, and chest pain. In severe cases, pneumonia can lead to serious complications such as respiratory failure, sepsis, and death.
Diagnosis of pneumonia typically involves a physical examination, medical history, and diagnostic tests such as chest X-rays or blood cultures. Treatment typically involves antibiotics to eliminate the infection, as well as supportive care to manage symptoms and prevent complications. Vaccines are also available to protect against certain types of bacterial pneumonia, particularly in children and older adults.
Preventative measures for bacterial pneumonia include:
* Getting vaccinated against Streptococcus pneumoniae and Haemophilus influenzae type b (Hib)
* Practicing good hygiene, such as washing hands regularly and covering the mouth and nose when coughing or sneezing
* Avoiding close contact with people who are sick
* Staying hydrated and getting enough rest
* Quitting smoking, if applicable
* Managing underlying medical conditions, such as diabetes or heart disease
It is important to seek medical attention promptly if symptoms of pneumonia develop, particularly in high-risk populations. Early diagnosis and treatment can help prevent serious complications and improve outcomes for patients with bacterial pneumonia.
List of MeSH codes (B03)
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i|Chlamydia muridarum|/i| infection differentially alters smooth muscle function in mouse uterine horn and cervix. | Am J...
Biocontainment Laboratory-Duke University School of Medicine, Duke Human Vaccine Institute | NIH: National Institute of Allergy...
DeCS - Termos Novos
Chlamydia (Chlamydial Genitourinary Infections): Background, Pathophysiology, Etiology
Role of innate and adaptive immunity in the outcome of primary infection with Chlamydia pneumoniae, as analyzed in genetically...
"Biol Reprod"[journal] - PMC -...
Caldwell HD - Search Results - PubMed
TREE NUMBER DESCRIPTOR
Loss of the interferon-γ-inducible regulatory immunity-related GTPase (IRG), Irgm1, causes activation of effector IRG proteins...
YRC Public Data Repository - Protein Structure Prediction - Protein Overview
Dynamic diversity of the tryptophan pathway in chlamydiae: reductive evolution and a novel operon for tryptophan recapture |...
SIGI: score-based identification of genomic islands | BMC Bioinformatics | Full Text
List Of Titles
Pre GI: CDS description
MGH DNA Core
A polyphosphate kinase (PPK2) widely conserved
Gels - Macrophage Inflammatory Proteins (MIP)
Adenoviridae - McMaster Experts
CDC Science Clips
Protocols and Video Articles Authored by Kathleen A. Kelly
Chlamydia pan-genomic analysis reveals balance between host adaptation and selective pressure to genome reduction | BMC...
NEW (2001) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; revised 9/6/2000
- They include the genera Chlamydia (of which the type species is Chlamydia trachomatis ) and Chlamydophila (eg, Chlamydophila pneumoniae and Chlamydophila psittaci ). (medscape.com)
- Other chlamydiae ( Chlamydia trachomatis, C. muridarum and Chlamydophila pneumoniae ) lack genes encoding PRPP synthase, kynureninase, and either lack tryptophan-pathway genes altogether or exhibit various stages of reductive loss. (biomedcentral.com)
- We find a larger potential for recombination in Chlamydophila pneumoniae genomes as compared with Chlamydia trachomatis or Chlamydia muridarum. (pasteur.fr)
- There are two genera in Chlamydiaceae: Chlamydia and Chlamydophila. (neobiolab.com)
- Chlamydia trachomatis are important agents of sexually transmitted disease as well as the main cause of preventable blindness in developing countries, and Chlamydia pneumoniae is one of the major causes of pneumonia worldwide. (biomedcentral.com)
Major outer membrane protein1
- We have evaluated proposed vaccine antigens in both models and observed immunization with Chlamydia major outer membrane protein (MOMP) vaccine formulations to be protective (p C. trachomatis model, and immunization with PmpD p82 translocator domain was not protective in either model. (scirp.org)
- Chlamydia muridarum infection differentially alters smooth muscle function in mouse uterine horn and cervix. (bvsalud.org)
- Chlamydia trachomatis infection is a primary cause of reproductive tract diseases including infertility . (bvsalud.org)
- This study characterized the physiological activities of the uterine horn and the cervix in a Chlamydia muridarum (Cmu)-infected mouse model at three infection time points of 7, 14, and 21 days postinfection (dpi). (bvsalud.org)
- The USPSTF recommends screening for chlamydia in sexually active females aged 24 years or younger and in older women who are at increased risk for infection. (medscape.com)
- Routine Chlamydia screening of sexually active young women is recommended to prevent consequences of untreated chlamydial infection (eg, pelvic inflammatory disease (PID), infertility , ectopic pregnancy , and chronic pelvic pain). (medscape.com)
- 4. Vaccination against chlamydial genital tract infection after immunization with dendritic cells pulsed ex vivo with nonviable Chlamydiae. (nih.gov)
- 14. Immunogenicity and protection against genital Chlamydia infection and its complications by a multisubunit candidate vaccine. (nih.gov)
- 16. Gene knockout B cell-deficient mice demonstrate that B cells play an important role in the initiation of T cell responses to Chlamydia trachomatis (mouse pneumonitis) lung infection. (nih.gov)
- 17. A genome-wide profiling of the humoral immune response to Chlamydia trachomatis infection reveals vaccine candidate antigens expressed in humans. (nih.gov)
- Letter to the editor re: in vivo whole animal body imaging reveals colonization of Chlamydia muridarum to the lower genital tract at early stages of infection. (edu.au)
- Chlamydia is a common term for infection with any bacterium belonging to the phylum Chlamydiae. (neobiolab.com)
- C. muridarum administered intravaginally in mice readily ascends to the upper genital tract  . (scirp.org)
- Chlamydiae are small gram-negative obligate intracellular microorganisms that preferentially infect squamocolumnar epithelial cells. (medscape.com)
- Chlamydiae have a unique biphasic life cycle that is adaptable to both intracellular and extracellular environments. (medscape.com)
- The chlamydiae are ubiquitous intracellular parasites that are important pathogens of humans and other organisms. (biomedcentral.com)
- Chlamydiae are obligate intracellular pathogens that infect a variety of host organisms and exhibit individual tissue tropisms within a host species. (biomedcentral.com)
- Chlamydia are ancient intracellular pathogens with reduced, though strikingly conserved genome. (biomedcentral.com)
- Bacteria of genus Chlamydia are intracellular pathogens of high medical significance. (biomedcentral.com)
- As a consequence of their obligatory intracellular lifestyle, Chlamydia have reduced genomes of about 1 Mb and 850-1100 genes. (biomedcentral.com)
- The E.coli derived recombinant 6x His fusion at C-terminus protein contains Chlamydia Trachomatis MOMP protein epitopes, 66-165 amino acids. (neobiolab.com)
- A highly conserved cryptic plasmid is present in Chlamydia trachomatis yet naturally occurring plasmid-deficient isolates are very rare. (nih.gov)
- 8. Differential sensitivity of distinct Chlamydia trachomatis isolates to IFN-gamma-mediated inhibition. (nih.gov)
- These isolates formerly belonged to CHLAMYDIA TRACHOMATIS . (nih.gov)
- The most common is the mouse model in which two different species of Chlamydiae are used: Chlamydia muridarum, originally isolated from the lungs of reportedly normal albino Swiss mice  , and human-derived Chlamydia trachomatis strains. (scirp.org)
- Species of CHLAMYDIA causing pneumonitis in mice and hamsters. (nih.gov)
- The genus Chlamydia includes three species: C. trachomatis, C. muridarum, and C. suis. (neobiolab.com)
- We report pan-genomic analysis of sixteen species from genus Chlamydia including identification and functional annotation of orthologous genes, and characterization of gene gains, losses, and rearrangements. (biomedcentral.com)
- Other chlamydial species infect a wide range of animals, and some of them (in particular, Chlamydia psittaci and Chlamydia abortus ) can cause life-threatening diseases if transmitted to humans [ 1 - 6 ]. (biomedcentral.com)
- Type species of CHLAMYDIA causing a variety of ocular and urogenital diseases. (nih.gov)
- Several animal models have been developed to evaluate Chlamydia infections and potential vaccines. (scirp.org)
- Chlamydia trachomatis is a ubiquitous human patho- Approximately 8%-57% of clinical STD samples gen that is responsible for the most prevalent bacte- mixed infections ( 5-7,9,12,13 ). (cdc.gov)
- 1. A live and inactivated Chlamydia trachomatis mouse pneumonitis strain induces the maturation of dendritic cells that are phenotypically and immunologically distinct. (nih.gov)
- This term derives from the name of the bacterial genus Chlamydiain the family Chlamydiaceae, order Chlamydiales, class and phylum Chlamydiae. (neobiolab.com)
- Cells present in the persistent state have been detected in vivo, for example, in the synovial membranes of patients with Chlamydia-associated reactive arthritis [ 8 ]. (biomedcentral.com)
- This paper describes the isolation and characterization of a plasmid-deficient strain of C. muridarum, using novobiocin as a curing agent. (nih.gov)
- Toll-like receptor 2 activation by Chlamydia trachomatis is plasmid dependent, and plasmid-responsive chromosomal loci are coordinately regulated in response to glucose limitation by C. trachomatis but not by C. muridarum. (nih.gov)
- Complete genomic sequences of closely related organisms, such as the chlamydiae, afford the opportunity to assess significant strain differences against a background of many shared characteristics. (biomedcentral.com)
- In 100% (42/42) of C. muridarum studies, mice immunized with Chlamydia elementary bodies (EB) demonstrated a significant reduction in urogenital bacterial shedding as measured by qPCR (p (scirp.org)
- Extracellular forms of Chlamydia ( elementary bodies ) attach to host cells and initiate endocytosis, yielding formation of a membrane-bound compartment termed the inclusion. (biomedcentral.com)
- Chlamydia trachomatis is the leading cause of prevent- reticulate bodies that multiply by binary fi ssion and redif- able blindness and bacterial sexually transmitted diseases ferentiate into EBs after 30-48 hours and then are released worldwide. (cdc.gov)
- Chlamydia vaccines: strategies and status. (nih.gov)
- Chlamydia W2 protein althoµgh stable at 4°C for 1 week, should be stored below -18°C. Please prevent freeze thaw cycles. (neobiolab.com)
- 3. A peptide of Chlamydia trachomatis shown to be a primary T-cell epitope in vitro induces cell-mediated immunity in vivo. (nih.gov)
- Chlamydia-induced pathology was present in mock-immunized animals, but at significantly greater levels in μmT than WT mice, whereas vaccinated μmT and WT mice exhibited similar reductions in pathology. (uthscsa.edu)
- We compared C. muridarum and C. trachomatis intravaginal challenge models in a combined total of seventy-five studies evaluating potential vaccine candidates. (scirp.org)
- Murine challenge models have been the most utilized animal model for Chlamydia trachomatis vaccine development. (scirp.org)
- Chlamydiae all progress through a life cycle that is intimately tied to success as a pathogen. (biomedcentral.com)
- A Chlamydia trachomatis vaccine would address a major global unmet medical need. (scirp.org)