Murine respiratory mycoplasmosis in F344 and LEW rats: evolution of lesions and lung lymphoid cell populations.

By comparison of two strains, LEW and F344, which are known to differ in susceptibility to Mycoplasma pulmonis respiratory disease, it was shown that differences in lesion severity and progression were associated with changes in lung lymphocyte populations. Lung lesions in LEW rats developed earlier after infection, became more severe, and were characterized by continued proliferation of all classes of lymphoid cells, T lymphocytes, B lymphocytes, and plasma cells, throughout the 120-day observation period. In contrast, lymphoid proliferation in F344 rats reached a plateau at 28 days and was restricted to an increase in T lymphocytes, immunoglobulin A (IgA)-bearing B lymphocytes, and IgA and IgG plasma cells. Although approximately 10 times as many IgG B cells and 4 times as many IgG plasma cells were found in infected LEW rats as compared with F344 rats, the specific anti-M. pulmonis IgG response in the two strains was roughly parallel. The same relationships held true, although to a lesser extent, for specific IgA antibody responses and cellular responses. Whereas lung lesions showed a tendency to resolve in F344 rats by 120 days, severe lesions persisted in LEW rats. The disparity between the cellular response and specific antibody response, the seemingly uncontrolled lymphocyte proliferation in LEW rats, and the mitogenic potential of M. pulmonis suggest that differences between LEW and F344 rats in lung lesion severity and progression are related to differences in the degree of nonspecific lymphocyte activation in the two strains, an imbalance in regulation of lymphocyte proliferation in LEW rats, or both.