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-Inducible Protein 10 and IFN-
Independent of TLR2 and TLR4, but Largely Dependent on MyD881
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* Division of Pediatric Infectious Diseases, Arkansas Children’s Hospital, Little Rock, AR 72202; Department of Microbiology and Immunology, University of Arkansas for Medical Sciences, Little Rock, AR 72205; Université Paris–Denis Diderot, Institut Jacques Monod, Paris, France; and School of Natural Sciences, University of California, Merced, CA 95344
IFN-
-inducible protein 10 (IP-10) is a chemokine important in the attraction of T cells, which are essential for resolution of chlamydial genital tract infection. During infections with Gram-negative bacteria, the IP-10 response mediated through type I IFNs usually occurs as a result of TLR4 stimulation by bacterial LPS. However, we found that levels of IP-10 in genital tract secretions of Chlamydia trachomatis-infected female wild-type mice were similar to those of infected TLR2- and TLR4-deficient mice but significantly greater than those of infected MyD88-deficient mice. We investigated the mechanism of IP-10 and IFN-
induction during chlamydial infection using mouse macrophages and fibroblasts infected ex vivo. The induction of IP-10 and IFN- was unchanged in Chlamydia-infected TLR2- and TLR4-deficient cells compared with wild-type cells. However, infection of MyD88-deficient cells resulted in significantly decreased responses. These results suggest a role for MyD88-dependent pathways in induction of IP-10 and IFN- during chlamydial infection. Furthermore, treatment of infected macrophages with an endosomal maturation inhibitor significantly reduced chlamydial-induced IFN-. Because endosomal maturation is required for MyD88-dependent intracellular pathogen recognition receptors to function, our data suggest a role for the intracellular pathogen recognition receptor(s) in induction of IFN- and IP-10 during chlamydial infection. Furthermore, the intracellular pathways that lead to chlamydial-induced IFN- function through TANK-binding kinase mediated phosphorylation and nuclear translocation of IFN regulatory factor-3.
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