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Chlamydia trachomatis  urogenital serovars primarily replicate in epithelial cells lining the reproductive tract. Epithelial cells recognize  Chlamydia  through cell surface and cytosolic receptors, and/or endosomal innate receptors such as Toll-like receptors (TLRs). Activation of these receptors triggers both innate and adaptive immune mechanisms that are required for chlamydial clearance, but are also responsible for the immunopathology in the reproductive tract. We previously demonstrated that  Chlamydia muridarum  ( Cm ) induces IFN-β in oviduct epithelial cells (OE) in a TLR3-dependent manner, and that the synthesis of several cytokines and chemokines are diminished in  Cm -challenged OE derived from TLR3 -/-  129S1 mice. Furthermore, our  in vitro  studies showed that  Cm  replication in TLR3 -/-  OE is more efficient than in wild-type OE. Because TLR3 modulates the release inflammatory mediators involved in host defense during  Cm  infection, we hypothesized that TLR3 plays a protective role against  Cm -induced genital tract pathology in congenic C57BL/6N mice. Using the  Cm  mouse model for human  Chlamydia  genital tract infections, we demonstrated that TLR3 -/-  mice had increased  Cm  shedding during early and mid-stage genital infection. In early stage infection, TLR3 -/-  mice showed a diminished synthesis of IFN-β, IL-1β, and IL-6, but enhanced production of IL-10, TNF-α, and IFN-γ. In mid-stage infection, TLR3 -/-  mice exhibited significantly enhanced lymphocytic endometritis and salpingitis than wild-type mice. These lymphocytes were predominantly scattered along the endometrial stroma and the associated smooth muscle, and the lamina propria supporting the oviducts. Surprisingly, our data show that CD4 +  T-cells are significantly enhanced in the genital tract TLR3 -/-  mice during mid-stage  Chlamydial  infection. In late-stage infections, both mouse strains developed hydrosalpinx; however, the extent of hydrosalpinx was more severe in TLR3 -/-  mice. Together, these data suggest that TLR3 promotes the clearance of  Cm  during early and mid-stages of genital tract infection, and that loss of TLR3 is detrimental in the development hydrosalpinx.

Toll-like receptor 3 (TLR3) promotes the resolution of Chlamydia muridarum genital tract infection in congenic C57BL/6N mice