Influenza A virus up-regulates neutrophil adhesion molecules and adhesion to biological surfaces

Influenza A virus (IAV) binds to sialylated neutrophil surface components (e.g., CD43 and sialyl Lewis(x) antigen) and induces both activation and functional depression of neutrophils. We report that IAV enhanced neutrophil adhesion to surfaces coated with serum or serum components, but not to uncoated plastic. IAV up-regulated expression of integrins (CD11b and CD11c) and carcinoembryonic-related antigens on neutrophils, while reducing expression of CD43, L-selectin, and P-selectin glycoprotein ligand (PSGL), Although treatment of neutrophils with elastase or O-sialoglycoprotease decreased surface CD43 and PSGL, they did not reduce binding of IAV to neutrophils, implying that IAV call bind to alternate binding sites in the absence of CD43. Pretreatment of neutrophils with elastase also did not prevent IAV from increasing expression of integrins and enhancing adhesion. Up-regulation of adhesion molecules slid adhesion are important, previously unrecognized, features of neutrophil activation by IAV, Further studies will be needed to clarify the mechanism of these effects.