Toll-like receptor 2 (TLR2), transforming growth factor-β, hyaluronan (HA), and receptor for HA-mediated motility (RHAMM) are required for surfactant protein a-stimulated macrophage chemotaxis

Abstract

Background: Surfactant protein A stimulates macrophage chemotaxis. Results: SPA interaction with TLR2 stimulates JNK- and ERK-dependent TGFβ production, which in turn stimulates RHAMM- and hyaluronan-dependent macrophage chemotaxis. Conclusion: SPA activates a novel and specific pathway to stimulate macrophage chemotaxis. Significance: Uncovering the mechanisms that regulate innate immunity in the lung is crucial for understanding the responses to infection and injury. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.