Studies of immunity to the pneumonitis agent of mice (murine Chlamydia trachomatis)

Pulmonary infection with Chlamydia trachomatis is a significant problem in infants and has been observed in the immunocompromised adult as well. The immunology of host defense against C. trachomatis, however, is poorly understood. To investigate this, we have employed a murine model of pneumonia and the mouse pneumonitis agent, a murine strain of C. trachomatis. This agent differs from human strains in DNA reassociation studies, but has the same base ratio and is much more virulent in mice than the usual human strains of C. trachomatis. We employed the nude (nu/nu) athymic mouse, known to be deficient in both T lymphocyte-dependent antibody production and cell-mediated immunity, and its furred, heterozygous (nu/+) littermate. Our studies to date have shown that the nu/nu mouse is significantly more susceptible to MoPn than the nu/+ mouse; remains culture positive (lung) for MoPn longer; does not make specific IgG or IgA antibody to MoPn (while the nu/+ mouse does); and cannot be successfully immunized against MoPn (whereas the nu/+ mouse is protected by immunization). Furthermore, passive transfer of immune nu/+ serum at day O significantly delayed mortality in nu/nu or nu/+ mice compared to controls given normal nu/+ serum demonstrating a role for antibody in host defense against MoP. The role of CMI in the model, however, remained unclear, and is the subject of these studies.