Characterization of lymphocyte response in the female genital tract duringascending chlamydial genital infection in the guinea pig model

It is well known that pathology caused by chlamydial infection is associate d closely with the host response to the organism and that both innate and a daptive host responses contribute to tissue damage. While it is likely that the organism itself initiates the acute inflammatory response by eliciting cytokine and chemokine production from the host cell, the adaptive respons e is the result of activation of the cell-mediated immune response. While t here are several studies describing the nature of the pathologic response i n primate, guinea pig, and murine models, there is less information on the kinetics of the CD4 and CD8 response following primary and challenge infect ions. In this study, we have quantified by flow cytometry the mononuclear c ell response to genital infection with the agent of guinea pig inclusion co njunctivitis in the cervix, endometrium, and oviducts at various times foll owing a primary intravaginal infection and after a challenge infection. Tis sues from individual animals were assessed for cells expressing CD4, CD8, o r Mac-1 and for B cells. Peak responses of each subset occurred 10 to 14 da ys after a primary infection. The number of Mac-1-expressing cells in each tissue site was found to be dependent on the size of the inoculating dose o f chlamydiae. The responses of each cell type were generally stronger in th e cervix than in the upper genital tract. In contrast to the murine model b ut consistent with the primate models, there were equal numbers of CD4 and CD8 cells present in the infiltrates. Twenty-one days after challenge infec tion, which was performed 50 days after the primary infection, there was a significant increase in the number of CD4, CD8, and B cells in the oviduct compared to the number of these cells at the same time after a primary infe ction, providing clear cellular evidence for a cell-mediated immune patholo gic response.