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Mycoplasmas are bacterial pathogens of a range of animals, including humans, and are a common cause of respiratory disease. However, the host genetic factors that affect resistance to infection or regulate the resulting pulmonary inflammation are not well defined. We and others have previously demonstrated that nonobese diabetic (NOD) mice can be used to investigate disease loci that affect bacterial infection and autoimmune diabetes. Here we show that NOD mice are more susceptible than C57BL/6 (B6) mice to infection withMycoplasma pulmonis , a natural model of pulmonary mycoplasmosis. The lungs of infected NOD mice had higher loads ofM. pulmonis and more severe inflammatory lesions. Moreover, congenic NOD mice that harbored different B6-derived chromosomal intervals enabled identification and localization of a new mycoplasmosis locus, termedMpr2 , on chromosome 13. These congenic NOD mice demonstrated that the B6 allele forMpr2 reduced the severity of pulmonary inflammation caused by infection withM. pulmonis and that this was associated with altered cytokine and chemokine concentrations in the infected lungs.Mpr2 also colocalizes to the same genomic interval asListr2 andIdd14 , genetic loci linked to listeriosis resistance and autoimmune diabetes susceptibility, respectively, suggesting that allelic variation within these loci may affect the development of both infectious and autoimmune disease.

Autoimmune-Disease-Prone NOD Mice Help To Reveal a New Genetic Locus for Reducing Pulmonary Disease Caused by Mycoplasma pulmonis