Housing conditions modulate the severity of Mycoplasma pulmonis infection in mice deficient in class A scavenger receptor.

摘要: Mycoplasmosis is a frequent causative microbial agent of community-acquired pneumonia and has been linked to exacerbation chronic obstructive pulmonary disease. The macrophage class A scavenger receptor (SRA) facilitates the clearance noxious particles, oxidants, infectious organisms by alveolar macrophages. We examined wildtype SRA(-/-) mice, housed in either individually ventilated or static filter-top cages that were cycled with fresh bedding every 14 d, as model gene-environment interaction on outcome Mycoplasma pulmonis infection. Intracage NH3 gas measurements recorded daily prior Mice intranasally infected 1 × 10(7) cfu M. UAB CT evaluated at 3, 7, d after inoculation. Wildtype mice cleared 99.5% 3 infection but remained chronically through study. SRA (-/-) 40-fold higher mycoplasma numbers than mice. caused mixed inflammatory response was accompanied high levels IL1β, KC, MCP1, TNFα whereas inflammation WT represented monocytosis elevation IL1β. Housing had prominent influence severity persistence mycoplasmosis an improved recovery significant changes surfactant proteins SPA SPD compared baseline levels. These results indicate required prevent lung. Furthermore, environmental conditions may exacerbate pulmonis-infected