Humoral Immune Response in Acquired Immunity to Chlamydial Genital Infection of Female Guinea Pigs

Rank, R. G.; Barron, Almen L.

doi:10.1128/iai.39.1.463-465.1983

Cited by 64 publications

(40 citation statements)

References 7 publications

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“…It is not difficult to conceive that women can become infected in the GI tract even in the absence of anal intercourse via fluid contamination of the rectum from the vagina or through oral sexual activity. Studies in all animal models demonstrate that genital infection resolves within several weeks through the development of a Th1 cell-mediated immune response (Rank, 2006). However, because T cells do not remain in the genital tract following recovery, the individual becomes susceptible to reinfection (Igietseme & Rank, 1991).…”

Section: Discussionmentioning

confidence: 99%

Chlamydial infection of the gastrointestinal tract: a reservoir for persistent infection

et al. 2013

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The mechanism by which chlamydiae persist in vivo remains undefined; however, chlamydiae in most animals persist in the gastrointestinal tract (GI) and are transmitted via the fecal-oral route. Oral infection of mice with Chlamydia muridarum was previously shown to establish a long-term persistent infection in the GI tract. In this study, BALB/c, DBA/2 and C57Bl/6 mice, infected orally with C. muridarum, were infected in the cecum for as long as 100 days in the absence of pathology. The primary target tissue was the cecum although the large intestine was also infected in most animals. A strong serum IgG and cecal IgA antibody response developed. Lymphocyte proliferation assays to chlamydial antigen on mesenteric lymph node cells were positive by day 10 and peaked on days 15–21, but the response returned to baseline levels by 50 days, despite the ongoing presence of the organism in the cecum. Since studies have shown that women and men become infected orally with chlamydiae, we propose that the GI tract is a site of persistent infection and that immune down-regulation in the gut allows chlamydiae to persist indefinitely. As a result, women may become reinfected via contamination of the genital tract from the lower GI tract.

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Section: Discussionmentioning

confidence: 99%

Chlamydial infection of the gastrointestinal tract: a reservoir for persistent infection

et al. 2013

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“…However, in laboratory animals other than the mouse there has been controversy for a number of years over the relative role of antibody or cell mediated immunity in protection. Few of these experiments could be regarded as definitive from a modern perspective, but it appears that in the guinea pig specific antibodies may play a more prominent role in protection compared to the mouse [23,[26][27][28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Studies in Knockout Mice Reveal that Anti‐Chlamydial Protection Requires TH1 Cells Producing IFN‐γ: Is this True for Humans?

et al. 1997

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Chlamydia trachomatis is one of the major causes of infertility and preventable blindness in the world. The organism is of particular interest from an immunological point of view because it is one of the few obligate intracellular bacterial pathogens. There is some evidence that repeated infections in humans stimulate protective immunity. However, until recently, it was unclear which components of the adaptive immune system give rise to protection. Studies in gene knockout mice reported here and elsewhere now give a coherent and cogent picture of the importance of the Th1 response, in particular IFN‐γ, for the localization and eradication of C. trachomatis genital tract infection. The key questions still to be addressed are the identity of the IFN‐γ responsive cells and whether the mouse is truly representative of host protection against chlamydiae in humans.

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“…While immunity appears to develop following a primary chlamydial genital infection, it is short-lived and individuals can be reinfected (4,17). Analyses of hosts' antichlamydial immune mechanisms in animal models have shown that in guinea pigs both humoral immunity (15,21) and cell-mediated immunity (16,20) are essential for resolution of and resistance to infection. However, in the murine system, several lines of evidence suggest that T-cell-mediated immunity is the principal immune mechanism for controlling chlamydial genital disease.…”

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Role for CD8+ T cells in antichlamydial immunity defined by Chlamydia-specific T-lymphocyte clones

et al. 1994

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The role of CD8+ T cells in antichlamydial immunity was investigated in a murine model of chlamydial genital infection by using T-cell clones generated against the Chlamydia trachomatis agent of mouse pneumonitis (MoPn). Two CD8+ T-cell clones tested (2.1F and 2.14-9) were chlamydia antigen specific and MHC restricted and reacted against MoPn as well as the Chlamydia psittaci agent of guinea pig inclusion conjunctivitis and C. trachomatis serovar E, suggesting the recognition of a genus-specific antigen. Upon adoptive transfer into persistently MoPn-infected nu/nu mice, 55.6% of the recipients of clone 2.1F (15 of 27) resolved the infection but recipients of clone 2.14-9 did not. The ability to resolve the MoPn infection correlated with the capacity of clone 2.1F to elaborate a combination of gamma interferon and tumor necrosis factor alpha. The results suggested that in addition to CD4+ T cells, CD8+ T cells may also contribute to antichlamydial T-cell immunity in vivo.

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Humoral Immune Response in Acquired Immunity to Chlamydial Genital Infection of Female Guinea Pigs

Cited by 64 publications

References 7 publications

Chlamydial infection of the gastrointestinal tract: a reservoir for persistent infection

Chlamydial infection of the gastrointestinal tract: a reservoir for persistent infection

Studies in Knockout Mice Reveal that Anti‐Chlamydial Protection Requires TH1 Cells Producing IFN‐γ: Is this True for Humans?

Role for CD8+ T cells in antichlamydial immunity defined by Chlamydia-specific T-lymphocyte clones

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