MyD88-dependent toll-like receptor signaling is required for murine macrophages response to IS2

IS2, a soluble beta-glucan isolated from the cell wall of mutated Saccharomyces cerevisiae (S. cerevisiae) enhances the immune response compared to the wild type (WT) beta-glucan. In the present investigation we report that Toll-like receptor (TLR)/MyD88 signaling pathway was responsible in IS2 beta-glucan-mediated cellular response in RAW264.7 murine macrophages. Data revealed that IS2 beta-glucan significantly up-regulated the TLR2/TLR4 expression. Moreover. TLR2/TLR4 responds to 152 resulting in murine macrophage activation. In addition, the IS2 signal led to cytokine secretions of IL-6 and TNF-alpha. In the case of thioglycolate-elicited peritoneal macrophages from MyD88-deficient mice, the decrease in cytokines was observed. Further the mitogen-activated protein kinases (MAPKs) phosphorylation was evident and degradation of I kappa B-alpha was increased after stimulation with IS2 beta-glucan. Further examination with MyD88-deficient mice revealed that the MyD88 pathway might play an important role for IS2 beta-glucan-mediated activation of macrophages. (C) 2011 Published by Elsevier B.V