S100A8 and S100A9 function as essential factors in inflammatory response and they induce cell differentiation, chemotactic activities, adhesion, apoptosis. In this study, I investigated the contribution of S100A8 and S100A9 to differentiation and chem...
S100A8 and S100A9 function as essential factors in inflammatory response and they induce cell differentiation, chemotactic activities, adhesion, apoptosis. In this study, I investigated the contribution of S100A8 and S100A9 to differentiation and chemotactic activity in the human eosinophilic cell line EoL-1. It is performed that a proliferation assay, chemotaxis assay and Western blotting. S100A8 and S100A9 increased the percentage of vacuole cell, the number of vacuole per one cell and the protein expression of EPO and MBP, indicating the differentiation of EoL-1 cells. S100A8 and S100A9-induced differentiation was inhibited by rottlerin, an inhibitor of protein kinase C delta (PKCδ). S100A8 and S100A9 induced the migration of EoL-1 cells and the migration was inhibited by TLR4, an inhibitor of TLR4, Ly2294002, an inhibitor of PI-3 kinase, AKTi, an inhibitor of AKT, rottlerin, PD98059, an inhibitor of ERK, SB202190, an inhibitor of p38 MAPK, SP600125, an inhibitor of JNK and BAY-11-7085, an inhibitor of NF-κB. S100A8 and S100A9 induced phosphorylation PKCδ, AKT, ERK, p38 MAPK, JNK and NF-κB in a time-dependent manner. The phosphorylation of ERK, p38 MAPK, JNK and NF-κB were inhibitied by TLR4i, Ly294002, AKTi and rottlerin. These findings contribute to an understanding of S100A8 and S100A9 in eosinophil biology and to the development of novel therapies for the treatment of allergy.