MyD88-dependent Toll-like receptor signaling is required for murine macrophages response to IS2
Hua Li ; Wan-Jae Kim ; Kwang-Ho Lee ; Dong-Kug Choi ; Pyo-Jam Park ; Sushruta Koppula ; Tae-Bong Kang ; Ji-Hwan Ryu ; Sang-Kyu Ye ; Tack-Joong Kim ; Eun-Yi Moon ; Hyung-Sun Youn ; Seung-Hwan Lee ; Jun Jiang
International Immunopharmacology, Vol.11(10) : 1578~1583, 2011
IS2, a soluble β-glucan isolated from the cell wall of mutated Saccharomyces cerevisiae (S. cerevisiae) enhances the immune response compared to the wild type (WT) β-glucan. In the present investigation we report that Toll-like receptor (TLR)/MyD88 signaling pathway was responsible in IS2 β-glucan-mediated cellular response in RAW264.7 murine macrophages. Data revealed that IS2 β-glucan significantly up-regulated the TLR2/TLR4 expression. Moreover, TLR2/TLR4 responds to IS2 resulting in murine macrophage activation. In addition, the IS2 signal led to cytokine secretions of IL-6 and TNF-α. 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 IκB-α was increased after stimulation with IS2 β-glucan. Further examination with MyD88-deficient mice revealed that the MyD88 pathway might play an important role for IS2 β-glucan-mediated activation of macrophages.