An experimental model for salpingitis due to Chlamydia trachomatis and residual tubal infertility in the mouse

“…For example, interleukin-6 (IL-6) was found to play a significant role in host defense against mouse lung infection (48), but not against genital tract infection (34), by C. muridarum. Since C. trachomatis-caused diseases in humans are in the urogenital tract and the C. muridarum-induced genital tract pathologies closely resemble those in the human genital tract induced by C. trachomatis infection (32,40,46,50), the C. muridarum urogenital infection mouse model has been widely used to study C. trachomatis pathogenesis and immune responses. Using this model, several groups have successfully mapped host adaptive immune components during resolution of chlamydial infection (25,26,33) and determined the role of Toll-like receptors in the innate immunity against chlamydial infection and the development of Chlamydia-induced pathologies (10).…”

mentioning

confidence: 99%

Caspase-1 Contributes toChlamydia trachomatis-Induced Upper Urogenital Tract Inflammatory Pathologies without Affecting the Course of Infection

Cheng¹,

Shivshankar²,

et al. 2008

Infect Immun

123

165

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Chlamydia trachomatis infection induces inflammatory pathologies in the upper genital tract, potentially leading to ectopic pregnancy and infertility in the affected women. Caspase-1 is required for processing and release of the inflammatory cytokines interleukin-1␤ (IL-1␤), IL-18, and possibly IL-33. In the present study, we evaluated the role of caspase-1 in chlamydial infection and pathogenesis. Although chlamydial infection induced caspase-1 activation and processing of IL-1␤, mice competent and mice deficient in caspase-1 experienced similar courses of chlamydial infection in their urogenital tracts, suggesting that Chlamydia-activated caspase-1 did not play a significant role in resolution of chlamydial infection. However, when genital tract tissue pathologies were examined, the caspase-1-deficient mice displayed much reduced inflammatory damage. The reduction in inflammation was most obvious in the fallopian tube tissue. These observations demonstrated that although caspase-1 is not required for controlling chlamydial infection, caspase-1-mediated responses can exacerbate the Chlamydia-induced inflammatory pathologies in the upper genital tract, suggesting that the host caspase-1 may be targeted for selectively attenuating chlamydial pathogenicity without affecting the host defense against chlamydial infection.

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“…Although severe tubal damage has long been considered as the major cause of female infertility resulting from genital C. trachomatis infection (3,4), 41% of women infected with C. trachomatis had endometrial infections (5). Little is known regarding possible post-C. trachomatis infection endometrial factor contributing to infertility and the underlying mechanism.…”

mentioning

confidence: 99%