Molecular mechanism of T‐cell control of Chlamydia in mice: role of nitric oxide in vivo

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T‐cell‐mediated immunity is crucial for the control of Chlamydia in mice. Recent evidence from studies in an in vitro model of the mucosal epithelium, the polarized epithelial–lymphocyte co‐culture (PELC) system, indicated that protective murine T cells mediated intracellular inhibition of the Chlamydia trachomatis agent of mouse pneumonitis (MoPn) at least partly by activating the interferon‐γ (IFN‐γ)‐inducible nitric oxide synthase (iNOS) pathway. To investigate whether nitric oxide played a role in controlling chlamydial infection in vivo, the protective capacity of a chlamydial‐specific T‐cell clone (clone 2.14‐0) was analysed in mice in the presence of a specific inhibitor of iNOS. The results revealed that the ability of this clone to clear Chlamydia in vivo is in part mediated by induction of nitric oxide (NO) production. The L‐arginine analogue and iNOS inhibitor, NG‐monomethyl‐L‐arginine monoacetate (MLA), increased the chlamydial burden in infected mice and inhibited the ability of clone 2.14‐0 to clear genital MoPn infection in vivo. The results are consistent with the working hypothesis that the IFN‐γ‐inducible iNOS pathway is involved in the control of Chlamydia by T lymphocytes in mice.