Tumor Necrosis Factor-α Mediates Antiapoptotic Signals Partially via p38 MAP Kinase Activation in Human EosinophilsTsukahara K. · Nakao A. · Hiraguri M. · Miike S. · Mamura M. · Saito Y. · Iwamoto I.
Department of Internal Medicine II, Chiba University School of Medicine, Chiba, Japan
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Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine with many biological effects on a variety of cells. In particular, TNF-α has been shown to act as a death or survival factor which mediates apoptosis or antiapoptotic signals in various types of cells. In eosinophils, TNF-α has been reported to activate eosinophil functions. However, it is not clearly defined whether TNF-α delivers antiapoptotic signals in eosinophils. In order to determine whether TNF-α prevents eosinophil apoptosis, we examined the effect of TNF-α on eosinophil apoptosis by the survival assay and cell cycle analysis. We also determined whether intracellular MAP kinases (ERKs, Jun kinase/JNK, and p38 MAP kinase) are involved in the TNF-α-induced signaling for the prevention of eosinophil apoptosis. We showed that TNF-α mediated antiapoptotic signals in human eosinophils in part via activation of p38 MAP kinase, but not via activation of ERKs and JNK. Our data suggest that TNF-α/p38 MAP kinase pathways are involved in the regulation of eosinophil survival and, thus, would be important for the development of allergic eosinophil-rich inflammation.
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