The role of immune cells in <i>Chlamydia</i>spread to the gastrointestinal tract following reproductive tract infection

Abstract Chlamydia trachomatisis the main cause of sexually transmitted disease and preventable blindness worldwide. In both animals humans, Chlamydiaspp. infect not only female reproductive tract (FRT), but also gastrointestinal (GIT), where it persists for long periods, without causing obvious pathology. murine model, following FRT infection, Chlamydiaspreads to GIT in stages relies on carriage by host cells. After initial infection epithelial cells FRT, lamina propria DCs internalize Chlamydia, which triggers their migration (and thus Chlamydiacarriage) FRT-draining iliac lymph nodes. ILNs, Chlamydiainfects other cells, which, then guided sphingosine 1-phosphate (S1P) gradient, enter circulation, carry Chlamydiato spleen GIT. Selective depletion either CD8 T or monocytes/macrophages significantly lowers Chlamydiaburden contrast, CD4 increases nodes While takes about one week Chlamydiaspread, ceca depleted mice become positive Chlamydiaby day 3 infection. It remains be determined whether infected actively transport GIT, simply limit (or allow) its growth at different affect Chlamydiaspread. Delineating interactions Chlamydiawith specific vivoand identifying chemokines that mediate Chlamydiaspread will shed light Chlamydiapathogenesis, regulation cell during Chlamydiainfection. Supported grant from NIH (1 R21 AI159743-01)