Animal cells and systems

  • 제13권4호
  • /
  • Pages.391-397
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  • 2009
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  • 1976-8354(pISSN)
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  • 2151-2485(eISSN)
한국통합생물학회 (The Korean Society for Integrative Biology)
권호 표지

Secretion of MCP-1, IL-8 and IL-6 Induced by House Dust Mite, Dermatophagoides pteronissinus in Human Eosinophilic EoL-1 Cells

  • Lee, Ji-Sook (Department of Biology, Daejeon University) ;
  • Kim, In-Sik (Department of Biomedical Laboratory Science, School of Medicine, Eulji University) ;
  • Yun, Chi-Young (Department of Biology, Daejeon University)
  • 발행 : 2009.12.31
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초록

The house dust mite (Dermatophagoides pteronissinus) is an important factor in triggering allergic diseases. The function of eosinophils, particularly in the production of cytokine or chemokine, is critical in understanding the pathogenesis of inflammatory diseases. In this study, we examined whether D. pteronissinus extract (DpE) induces the expression of monocyte chemotactic protein 1 (MCP-1)/CCL2, IL-8/CXCL8, and IL-6 that mediate in the infiltration and activation of immune cells and in its signaling mechanism in the human eosinophilic cell line, EoL-1. DpE increased the mRNA and protein expression of MCP-1, IL-8, and IL-6 in a time- and dose-dependent course in EoL-1 cells. In our experiments using signal-specific inhibitors, we found that the increased expression of MCP-1, IL-8, and IL-6 due to DpE is associated with Src family tyrosine kinase and protein kinase C $\delta$ (PKC $\delta$). In addition, the activation of extracellular signal-regulated kinase (ERK) is required for MCP-1 and IL-8 expression while p38 mitogen-activated protein kinase (MAPK) is involved in IL-6 expression. DpE induced the phosphorylation of ERK and p38 MAPK. PP2, an inhibitor of Src family tyrosine kinase, and rottlerin, an inhibitor of PKC $\delta$, blocked the activation of ERK and p38 MAPK. DpE induces the activation of ERK and p38 MAPK via Src family tyrosine kinase and PKC $\delta$ for MCP-1, IL-8, or IL-6 production. Increased cytokine release due to the house dust mite and the characterization of its signal transduction may be valuable in understanding the eosinophil-related pathogenic mechanism of inflammatory diseases.

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