Sexually transmitted
Chlamydia trachomatis
can ascend to the upper genital tract due to its resistance to innate immunity in the lower genital tract.
C. trachomatis
can activate cGAS-STING signaling pathway in cultured cells via either cGAS or STING. The current study was designed to evaluate the role of the cGAS-STING pathway in innate immunity against
C. trachomatis
in the mouse genital tract. Following intravaginal inoculation,
C. trachomatis
significantly declined by day 5 following a peak infection on day 3 while the mouse-adapted
C. muridarum
continued to rise for >1 week, indicating that
C. trachomatis
is susceptible to the innate immunity in the female mouse genital tract. This conclusion was supported by the observation of a similar shedding course in mice deficient in adaptive immunity. Thus,
C. trachomatis
can be used to evaluate innate immunity in the female genital tract. It was found that mice deficient in either cGAS or STING significantly increased the yields of live
C. trachomatis
on day 5, indicating an essential role of the cGAS-STING signaling pathway in innate immunity of the mouse genital tract. Comparison of live
C. trachomatis
recovered from different genital tissues revealed that the cGAS-STING-dependent immunity against
C. trachomatis
was restricted to the mouse lower genital tract regardless of whether
C. trachomatis
was inoculated intravaginally or transcervically. Thus, we have demonstrated an essential role of the cGAS-STING signaling pathway in innate immunity against chlamydial infection, laying a foundation for further illuminating the mechanisms of the innate immunity in the female lower genital tract.
Clinicopathologic Study of Hematologic Malignancies Involving the Female Genital Tract and a Role of Additional Immunohistochemistry in Discriminating Between Primary and Secondary Cases
