Beta 2 Microglobulin and Resistance to Murine Respiratory Mycoplasmosis

Mycoplasma pulmonis (MP) infection causes murine respiratory mycoplasmosis (MRM) in mice. This study was designed to determine whether C57BL/6 beta 2 microglobulin knockout (KO) mice (2m^-/-) differed from C57BL/6 2m^+/+ wild-type (WT) mice in the early events of acute infection and to confirm previous studies that suggested loss of beta 2 microglobulin (2m) expression was correlated with increased disease susceptibility. Experimentally infected mice were necropsied at various time points after infection. Quantitative cultures were performed on lung, trachea, and nares at each time point. Tissues were collected for histopathology. Both genotypes had marked clearance of MP from all sites within the first 24 h post-infection (p.i.). There were no differences between KO and WT mice in the ability to clear MP from the lung, nares, or trachea during the first 48 h p.i. During chronic infection, there was a significant difference among days p.i. for number of MP isolated from the lungs, nares, and trachea (P < 0.05). There were significant differences (P < 0.05) between genotypes for number of MP isolated from the lung. Numbers of MP isolated from KO mice were greater than from WT mice at day 10 through day 28 p.i. There was no significant overall difference between genotypes for number of MP isolated from the nares or trachea. However, increased numbers of MP were isolated from the nares of KO mice at days 21 and 28 p.i. and from the trachea of KO mice at days 7 and 21 p.i. During chronic infection, KO mice had increased facial scratching and altered respiration as well as marked weight loss compared with those of WT mice. The KO and WT mice differed (KO more severe) with respect to the presence and extent of neutrophilic exudate in the lung. Differences approached significance for consolidation of lung parenchyma but not for lymphoid infiltration, tending to be more severe in KO mice. Loss of 2m does not appear to affect clearance of MP during the critical first 48 h of infection but does seem to affect chronic infection, which may be because of the loss of CD8⁺Tc1 cells, the CD1–2m complex, or both.