Identification and analysis of host cell responses to infection with Chlamydia trachomatis

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University of Birmingham , Birmingham
Statementby Andrew Devitt.
ID Numbers
Open LibraryOL22278504M

Abstract. To study the responses of the host cell to chlamydial infection, differentially transcribed genes of the host cells were examined. Complementary DNA (cDNA) probes were made from messenger RNAs of HeLa cells infected with Chlamydia trachomatis and were hybridized to a high-density human DNA microarray of 15, genes and expressed sequence by: Interactions between Chlamydia trachomatis and the Host Cell With approximately 90 million cases occurring worldwide, the Gram-negative obligate intracellular pathogen, Chlamydia trachomatis, can be considered to be the most commonly transmitted bacterial sexually transmitted clearing of an infection, women can develop tubal infertility, pelvic inflammatory.

Dendritic cells are central for the induction of T cell responses needed for chlamydial eradication. Here we report the activation of two dendritic cell subsets: a classical, CD11b+ (cDC) and plasmacytoid (pDC) during genital infection with C.

l infection induced influx of cDC and pDC into the gential tract (GT) and its draining lymph node (ILN) as well as co-localization with Cited by: Genital infections with Chlamydia trachomatis continue to be a major health problem worldwide.

While some individuals clear their infection (presumed to be the result of an effective Th1/interferon-γ response), others develop chronic infections and some are prone to repeat infections. In females in particular, chronic asymptomatic infections are common and can lead to pelvic inflammatory Cited by:   The extracellular chlamydial infectious particle, or elementary body (EB), is enveloped by an intra- and intermolecular cysteine cross-linked protein shell called the chlamydial outer membrane complex (COMC).

A few abundant proteins, including the major outer membrane protein and cysteine-rich proteins (OmcA and OmcB), constitute the Identification and analysis of host cell responses to infection with Chlamydia trachomatis book majority of COMC by: The obligate intracellular bacterium Chlamydia trachomatis replicates in a cytosolic vacuole in human epithelial cells.

Infection of human cells with matis causes substantial changes to many host cell‐signalling pathways, but the molecular basis of such influence is not well understood. Studies of gene transcription of the infected cell have shown altered transcription of many host.

The first and most important immune response to Chlamydia infection is a local one, whereby immune cells such as leukocytes are recruited to the site of infections, and subsequently secrete pro. Chlamydia trachomatis (Ct) is responsible for the majority of bacterial sexually transmitted infections worldwide [].In addition, ocular Ct infections (trachoma) are the world’s leading cause of preventable blindness [2, 3].Although there are few documented reports of antibiotic resistance in Ct and infections can be easily treated, the persistent rates of Ct globally, makes this infection.

trachomatis replicates only inside a vacuole, termed inclusion, in the cytoplasm of the host cell (Fig. The mucosal epithelial cells are the primary target cell type in vivo. For most C. trachomatis strains, infection is limited to the mucous membrane, although lymphogranuloma venereum (LGV) strains attack deep lymphatic tissues.

Chlamydia trachomatis (Ct) infection is the commonest bacterial sexually transmitted infection worldwide (Howie et al., a, b). In the under age group in the UK 7–8% of men and women are infected. 70% of women and 50% of men who have Ct infection have no symptoms (Manavi, ); therefore if they do not get tested and treated, they can continue spreading the disease.

Recently, it was demonstrated that CD8+ T cells are important for the response against Chlamydia pneumoniae. By use of the human monocytic cell line U and human monocytes taken from peripheral. Chlamydia cultivation. trachomatis serovar L2 (strain /Bu) was cultivated in HeLa cells, and EB were purified by Renografin density gradient (DG) centrifugation as previously described ().EB were enumerated by dilution titration on HeLa cells and were visualized by immunofluorescent microscopy using the monoclonal antibody EVI-H1, which targets chlamydial LPS ().

Chlamydia are obligate intracellular bacteria that modulate apoptosis of the host cell. Strikingly, chlamydial infection has been reported both to inhibit and to induce apoptosis. Although the ability to inhibit apoptosis has been corroborated by the identification of cellular targets, confirmation of cell death induction has been complicated by a mixture of apoptotic features and atypical.

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dying infected cells were efficiently taken up by professional phagocytes, suggesting that Chlamydia-induced host-cell death could play a role in the immune response. In conclusion, chlamydial infection can induce cell death.

Although Chlamydia-induced cell death has certain morphological features of apoptosis, it does not. Adhesion. Efficient adhesion to host cells is a prerequisite for invasion and intracellular life and usually requires several adhesins.

Chlamydia has evolved a number of ways to attach to various host cells and infect different tissues according to serovariant and species [29,30].Early research focused on the role of the abundant major outer membrane protein (MOMP) as an adhesin [] (Figure 1 A-B).

ested reader to a recently published book [28]. Adhesion Efficient adhesion to host cells is a prerequisite for invasion and intracellular life and usually requires several adhesins. Chlamydia has evolved a number of ways to attach to vari-ous host cells and infect different tissues according to.

Details Identification and analysis of host cell responses to infection with Chlamydia trachomatis EPUB

Chlamydia trachomatis is an important human pathogen and the best investigated member of the order Chlamydiales[].Infection with C. trachomatis is among the most frequent causes of sexual transmitted diseases (STD). Infections of the upper inner eyelid eventually leading to scarring blindness (trachoma) are worldwide among the most frequently occurring ocular infections with.

The obligate intracellular bacterial pathogen Chlamydia trachomatis is reliant on a developmental cycle consisting of two cell forms, termed the elementary body (EB) and the reticulate body (RB).

The EB is infectious and utilizes a type III secretion system and preformed effector proteins during invasion, but it does not replicate. The RB replicates in the host cell but is noninfectious.

Tissue culture and bacterial culture conditions. Chlamydia trachomatis serovar L2 (L2//Bu) was cultured in HeLa or L cells as previously described (). pneumoniae (CWL) was grown on Hep2 cells by centrifuging inoculum onto monolayers at × g for 1 h at 24°C.

After a 1-h incubation at 37°C, RPMI (Invitrogen, Carlsbad, CA) containing 5% fetal bovine serum (FBS; HyClone, Logan. Infection with the bacterium Chlamydia trachomatis can lead to a variety of diseases, including ectopic pregnancy, infertility and blindness.

Exposure of the host to C. trachomatis stimulates multiple innate and adaptive immune effectors that can contribute towards controlling bacterial replication. However, these effectors are often insufficient to resolve the infection and prevent re.

In a preliminary study to investigate whether these genes are involved in the koala immune response to infection by its chlamydial pathogen, C.

pecorum, we investigated the expression of four genes in koalas with active chlamydia infection, those with past infection and those without infection using qPCR. This analysis revealed that one of. trachomatis infected host cells resist polyI:C‐induced apoptosis in an moi‐dependent manner.

We investigated the chlamydial inhibition of apoptosis induced by polyI:C, a synthetic dsRNA that is a potent activator of cytoplasmic RNA sensors, such as the RNA‐dependent protein kinase (PKR), to reveal the influence of an infection with C.

trachomatis on the cell's response to a viral co. Chlamydia spp. have been shown to both induce and inhibit host cell apoptosis, depending on the stage of the chlamydial developmental cycle. 13 Chlamydiae protect infected cells against apoptosis as a result of external stimuli during early stages of infection and may induce apoptosis of the host cell during later stages of the life cycle.

Description Identification and analysis of host cell responses to infection with Chlamydia trachomatis PDF

Thus. () A Chlamydia pneumoniae adhesin induces phosphatidylserine exposure on host cells. Nature Communications. doi. org/ / s Posted in: Medical Research News | Disease. Immunopathology after Chlamydia trachomatis infection is the major cause of human suffering associated with this pathogen, yet the immune responses that drive pathology are not well defined.

We demonstrate that a mucosal influx of neutrophils and CXCR3-driven CD4+ and CD8+ T cells is required for C. trachomatis pathology and does not contribute to bacterial clearance. Chlamydia pneumoniae is an important obligate intracellular pathogen that replicates within an inclusion in the eukaryotic cell.

The initial event of a chlamydial infection is the adherence to and subsequent uptake of the infectious elementary bodies (EBs) by the human cell.

These processes require yet-unidentified bacterial and eukaryotic surface proteins. This chapter discusses the possible role of gamma interferon (IFN-γ) and heat shock proteins (Hsps) in the pathogenesis of chlamydial disease. It reviews preliminary evidence from trachoma and pelvic inflammatory disease (PID) suggesting that human genotype exerts a substantial influence.

It discusses some of the evidence behind current concepts of chlamydial disease mechanisms, and focuses. Chlamydia trachomatis is an obligate intracellular human bacterial pathogen that infects epithelial cells of the eye, oropharynx, urogenital, and anorectal mucosa and is responsible for the clinical diseases of trachoma, chlamydia (urogenital, oropharyngeal, and anorectal), and lymphogranuloma venereum.C.

trachomatis infections occur worldwide and infection rates are increasing. The obligate intracellular bacterial pathogen Chlamydia trachomatis (Ctr) has been associated with cervical and ovarian cancer development.

However, establishment of causality and the underlying mechanisms remain outstanding. Our analysis of Ctr-induced alterations to global host histone modifications revealed distinct patterns of histone marks during acute and persistent infections. In another study to identify bacterial secreted proteins, immunofluorescence assays with antisera raised against Cpn and Cpn showed signals that were distributed within the host cell rather than inside the inclusions, implying that these are proteins secreted by the bacteria to modify host response.

The influence of chlamydial. Chlamydia trachomatis is a gram-negative obligate intracellular pathogen of the Chlamydiacae family. Originally thought to be a virus, because of the organism’s dependence on key metabolic intermediates (including ATP) from biosynthetic pathways of the eukaryotic host, C.

trachomatis is now known to have a cell wall, DNA, RNA, and ribosomes and is classified as Bacteria. McCoy cells infected with Chlamydia trachomatis serovars E or L2 revealed, by indirect immunofluorescence microscopy, collocation of microtubules and Chlamydia‐containing vesicles during the process of migration from the host cell surface to a perinuclear location.Chlamydia pneumoniae is a common cause of community-acquired pneumonia and it has been associated with atherosclerosis.C.

pneumoniae has usually been diagnosed by serology using a microimmunofluorescence test, but more recently polymerase chain reaction (PCR) has been viewed as an advantageous alternative. We developed a quantitative real-time PCR for detection of C. .