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

Abstract

By comparison of two rat 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.

Mechanism of antigenic variation in Mycoplasma pulmonis: interwoven, site‐specific DNA inversions

“…Identification of a DNA inversion system in the M. pulmonis vsa locus M. pulmonis strain UAB 6510 is a respiratory pathogen of rats (Davis et aL, 1982) that served as the progenitor of the other strains used in this study. A description of the lineage and pertinent properties of these strains is provided in the Experimental procedures.…”

Vaccination of Lewis rats with temperature-sensitive mutants of Mycoplasma pulmonis: adoptive transfer of immunity by spleen cells but not by sera

“…In contrast, immune cells protect against experimental infection in genetically resistant F344 strain rats (2). It has been reported that there are differences in the responses of rat strains F344 and LEW (7,10,11) and various mouse strains (9,24) to infection with M. pulmonis. The differences in the relative importance of cellular and antibody-mediated mechanisms of resistance to M. pulmonis may have been related to strain (resistant versus susceptible) rather than species differences (14).…”

“…Numerous cells infiltrate lungs of rats and mice following M. pulmonis infection (4,8,11). A significant number of cells (about 50% in tissue sections) were morphologically indistinguishable from lymphocytes, which failed to stain with either Tor B-cell reagents, and were called null cells.…”

Respiratory Tract

“…In the Lewis strain this was characterized after 28 days by a variable acute inflammatory exudate in bronchi and bronchioles with focal bronchiectasis, inflammation and hyperplasia of the epithelium with a predominantly macrophage infiltration of the alveoli and alveolar walls. 65,143 These changes were associated with marked hyperplasia of the bronchus-associated lymphoid tissue (BALT), which extended down the airways and blood vessels towards the periphery of the lungs. Although the lymphoid hyperplasia was also found in inoculated Fischer 344 rats, it was less marked and accompanied by little or no mucopurulent exudate or active inflammation of the bronchial walls.…”

“…This disparity in response suggested that differences were related to the degree of lymphocyte activation in the two strains, an imbalance in regulation of lymphocyte proliferation in Lewis rats, or both. 143 Other studies have been conducted in both rats and mice infected with another important respiratory pathogen of laboratory rodents, the Sendai virus (parainfluenza type 1). Sequential studies showed that the initial damage to bronchial and bronchiolar epithelium is associated with polymorphonuclear and lymphocytic inflammation (bronchiolitis).…”