Modulation of infection-mediated migration of neutrophils and CXCR2 trafficking by osteopontin

摘要: Osteopontin (OPN) is a pro-inflammatory protein that paradoxically protects against inflammation and bone destruction in mouse model of endodontic infection. Here we have tested the hypothesis this effect OPN mediated by effects on migration innate immune cells to site Using air pouch as infection mice, showed neutrophil accumulation at with mixture pathogens significantly reduced OPN-deficient mice. Reduced absence was accompanied an increase bacterial load. OPN-deficiency did not affect survival, CXCR2 ligand expression, or production inflammatory cytokines pouch. In vitro, enhanced CXCL1, whereas vivo, inhibition suppressed cellular infiltration pouches infected wild-type mice > 50%, but had no increased cell surface expression marrow neutrophils integrin-αv -dependent manner, internalization ligand. Together, these results support where protective from initial sites resulting optimal killing. We describe novel mechanism for OPN: suppression neutrophils, which increases ability migrate response ligands.