Roles of Innate and Adaptive Immunity in Respiratory Mycoplasmosis

Abstract

Current evidence suggests that host defense in respiratory mycoplasmosis is dependent on both innate and humoral immunity. To further delineate the roles of innate and adaptive immunity in antimycoplasmal defenses, we intranasally infected C3H/HeSnJ-scid/scid (C3H-SCID), C3H/HeSnJ (C3H), C57BL/6J-scid/scid (C57-SCID), and C57BL/6N (C57BL) mice with Mycoplasma pulmonis and at 14 and 21 days postinfection performed quantitative cultures of lungs and spleens, quantification of lung lesions, and histopathologic assessments of all other major organs. We found that numbers of mycoplasmas in lungs were associated with genetic background (C3H susceptible, C57BL resistant) rather than functional state of adaptive immunity, indicating that innate immunity is the main contributor to antimycoplasmal defense of the lungs. Extrapulmonary dissemination of mycoplasmas with colonization of spleens and histologic lesions in multiple organs was a common occurrence in all mice. The absence of adaptive immune responses in severe combined immunodeficient (SCID) mice resulted in increased mycoplasmal colonization of spleens and lesions in extrapulmonary sites, particularly spleens, hearts, and joints, and also reduced lung lesion severity. The transfer of anti-M. pulmonis serum to infected C3H-SCID mice prevented extrapulmonary infection and disease, while the severity of lung lesions was restored by transfer of naive spleen cells to infected C3H-SCID mice. Collectively, our results strongly support the conclusions that innate immunity provides antimycoplasmal defense of the lungs and humoral immunity has the major role in defense against systemic dissemination of mycoplasmal infection, but cellular immune responses may be important in exacerbation of mycoplasmal lung disease.

Defective Fas ligand-mediated apoptosis predisposes to development of a chronic erosive arthritis subsequent toMycoplasma pulmonis infection

“…This inflammation was cleared from all of these tissues by week 4. This supports the observation that the B6 mouse strain is resistant to the M pulmonis– induced persistent inflammatory response (34, 43, 44). For B6‐ lpr / lpr and B6‐ gld / gld mice, after infection with M pulmonis , there was a persistent interstitial infiltration in the lung, liver, and kidney that was similar to the persistent inflammation in the joints.…”

“…To clarify whether the chronic arthritis observed in B6‐ lpr / lpr and B6‐ gld / gld mice was due to a defect in the clearance of M pulmonis from the joints (knee and elbow), we determined the degree of recovery of Mycoplasma in B6‐ +/+ , B6‐ gld / gld , and B6‐ lpr / lpr mice. Since Cartner et al (34) have previously reported that the spleen is susceptible to mycoplasma infection after systemic dissemination, we also determined the rate of recovery of mycoplasma from the spleens of infected mice.…”

Mycoplasma pneumoniae Induces Host-Dependent Pulmonary Inflammation and Airway Obstruction in Mice

“…This emphasizes that the immunogenetic background (mouse strain) is important for the development of M. pneumoniaeassociated AHR. A variety of infectious disease models demonstrate variable host genetic susceptibility to disease expression (22,23,(37)(38)(39)(40). In such models, variation in susceptibility has frequently been correlated with differences in the patterns of immune responses.…”

Biology and Diseases of Mice

“…Prevention and control. Mice mount an effective immune response to Mycoplasma pulmonis, as measured by their recovery from mild infection and their resistance to infection after active or passive immunization (Cartner et al, 1998). Antibodies of various classes are produced locally and systemically, but their role in infection is unclear.…”