Murine respiratory mycoplasmosis resulting from Mycoplasma pulmonis infection in rats provides a useful model for the study of immunological and inflammatory mechanisms operative in the respiratory tract. We have previously shown that LEW rats develop more severe disease than do F344 rats. To further study the production of antibody responses in chronic respiratory disease due to M. pulmonis infection, we examined the distribution and development of M. pulmonis-specific antibody-forming cells (AFC) in different segments of the respiratory tracts of infected LEW and F344 rats. In these studies, the upper respiratory nodes were the initial site of antibody production after infection and remained the major site for recovery of AFC. Since infected LEW rats had equal or higher numbers of AFC than did infected F344 rats, these results suggest that the level of local antibody production alone is not responsible for the decreased susceptibility of F344 rats to murine respiratory mycoplasmosis. The differences in total antibody responses appear to be due to the greater numbers of cells recovered from the tissues of infected LEW rats compared with those recovered from F344 rats, suggesting that LEW rats may have greater production of chemotactic factors. Also, we demonstrate that nonspecific activation and/or recruitment of B cells occurs in the respiratory tracts of both LEW and F344 rats after infection with M. pulmonis.
|Number of pages||7|
|Journal||Infection and Immunity|
|State||Published - 1991|