Because epithelial cells are the major cell type productively infected with Chlamydia during genital tract infections, the overall goal of our research is to understand the contribution of the infected-epithelial cells to the host defense. We showed that TLR3 is the critical PRR in oviduct epithelial (OE) cells that is stimulated during Chlamydia infection, resulting in the synthesis of IFN-β. Our ELISA data indicate that expression of other innate immune modulators including IL-6, CXCL-10, CXCL-16, and CCL-5 were induced in the infected wild-type OE cells; however, this induction was not observed in the TLR3-deficient OE cells. Pre-treatment of the TLR3-deficient OE cells with 50 U/ml IFN-β prior to infection restored the ability of Chlamydia infection to induce IL-6, CXCL10, and CCL-5 expression; however CXCL-16 induction was not restored by IFN-β pre-incubation in the TLR3-deficient cells. Our findings were corroborated in pathway-focused PCR arrays which demonstrated a plethora of different inflammatory genes that were defectively regulated during Chlamydia infection of the TLR3-deficient OE cells, and that some of these genes were induced only when IFN-β was added prior to infection. Our OE cell data implicate TLR3 as an essential inducer of INF-β and other inflammatory mediators during Chlamydia infection, and highlights the importance of the role of TLR3 during the inflammatory cytokine response.
- Copyright © 2011 by The American Association of Immunologists, Inc.