Tec kinases regulate actin assembly and cytokine expression in LPS-stimulated human neutrophils via JNK activation

Rachel L. Zemans, Patrick G. Arndt

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

The acute inflammatory response involves neutrophils wherein recognition of bacterial products, such as lipopolysaccharide (LPS), activates intracellular signaling pathways. We have shown that the mitogen-activated protein kinase (MAPK) c-Jun NH2 terminal kinase (JNK) is activated by LPS in neutrophils and plays a critical role in monocyte chemoattractant protein (MCP)-1 expression and actin assembly. As the Tec family kinases are expressed in neutrophils and regulate activation of the MAPKs in other cell systems, we hypothesized that the Tec kinases are an upstream component of the signaling pathway leading to LPS-induced MAPKs activation in neutrophils. Herein, we show that the Tec kinases are activated in LPS-stimulated human neutrophils and that inhibition of the Tec kinases, with leflunomide metabolite analog (LFM-A13), decreased LPS-induced JNK, but not p38, activity. Furthermore, LPS-induced actin polymerization as well as MCP-1, tumor necrosis factor-α, interleukin-6, and interleukin-1β expression are dependent on Tec kinase activity.

Original languageEnglish (US)
Pages (from-to)90-97
Number of pages8
JournalCellular Immunology
Volume258
Issue number1
DOIs
StatePublished - 2009

Bibliographical note

Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.

Keywords

  • Cell signaling
  • Lipopolysaccarhide
  • MAP kinase
  • MCP-1
  • Neutrophil

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