The scavenger receptor B1, known for its regulation of high-density lipoprotein complexes in plasma and uptake of vitamin E, is expressed in AMs and epithelial cells, but its role in lung immune responses has not been explored. In Mucosal Immunology, Gowdy et al. show that SR-B1 is required for host survival in settings of bacterial pneumonia. SR-B1-deficient mice fail to control infection with Klebsiella pneumoniae despite developing neutrophilia and expressing more TNF and CXCL5 in their infected lung tissues than do similarly infected wild-type mice. Their bacterial counts are systemically higher, which indicates that loss of local control contributes to dissemination of the pathogen and sepsis. SR-B1-deficient neutrophils show defects in the clearance of lipopolysaccharide, bacterial phagocytosis and killing. The last defect is associated with deficient generation of reactive oxygen species by the intracellular NADPH oxidase complex. These findings should spur further research into how scavenger receptors influence immunity.
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Dempsey, L. Scavenger receptor B1 in lung immunity. Nat Immunol 16, 64 (2015). https://doi.org/10.1038/ni.3068
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DOI: https://doi.org/10.1038/ni.3068
