期刊
INFECTION AND IMMUNITY
卷 90, 期 4, 页码 -出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/iai.00651-21
关键词
Chlamydia; IL-27; IL-27R; inhibition; Th1; genital tract infection
资金
- U.S. National Institutes of Health [R01AI047997, R01AI153506]
- Natural Science Foundation of China [31670178]
In this study, it was found that IL-27 may promote chlamydial infection in the female mouse genital tract and increase chlamydial burden by suppressing IFN-gamma-mediated immunity. Knocking out IL-27R from T cells alone significantly shortened the infectious shedding courses of Chlamydia in the mouse genital tract. These findings suggest that attenuating IL-27 signaling in T cells may be used to enhance genital tract immunity against chlamydial infection.
Intravaginal infection of mice with Chlamydia muridarum has been used for investigating the mechanisms of Chlamydia rrachomaris-induced pathogenicity and immune responses. In the current study, the mouse model was used to evaluate the impact of interleukin-27 (IL-27) and its receptor signaling on the susceptibility of the female genital tract to chlamydial infection. Mice deficient in IL-27 developed significantly shortened courses of chlamydial infection in the female genital tract. The titers of live Chlamydia recovered from the genital tract of IL-27-deficient mice declined significantly by day 7 following intravaginal inoculation. These observations suggest that IL-27 may promote chlamydial infection in the female mouse genital tract. This conclusion was validated using IL-27 receptor (R)-deficient mice. Further, the reduction in chlamydial burden corelated with the increase in gamma interferon (IFN-gamma) and IL-17 in the genital tract tissues of the IL-27R-deificent mice. However, depletion of IFN-gamma but not IL-17 from the IL-27R-deificent mice significantly increased the chlamydial burden, indicating that IL-27 may mainly suppress IFN-gamma-mediated immunity for promoting chlamydial infection. Finally, knockout of IL-27R from T cells alone was sufficient for significantly shortening the infectious shedding courses of Chlamydia in the mouse genital tract. The above-described results have demonstrated that Chlamydia can activate IL-27R signaling in Th1-like cells for promoting its infection in the female genital tract, suggesting that attenuating IL-27 signaling in T cells may be used for enhancing genital tract immunity against chlamydial infection.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据