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Induction of TNF-alpha by LPS in Schwann cell is regulated by MAPK activation signals

Chun Cheng1, Yongwei Qin, Xiaoyi Shao

  • 1Key Laboratory for Neuroregeneration of JiangSu Province, Nantong University, 19 Qixiu Road, Nantong 226001 Jiangsu, PR China.

Cellular and Molecular Neurobiology
|September 29, 2007
PubMed

Insights

Lipopolysaccharide (LPS) from gram-negative bacteria activates mitogen-activated protein kinases (MAPKs) and tumor necrosis factor-alpha (TNF-alpha) in Schwann cells (SCs). This immune response is crucial for understanding cellular reactions to bacterial components.

Area of Science:

  • Neuroimmunology
  • Cellular and Molecular Biology

Background:

  • Mitogen-activated protein kinases (MAPKs) are key in immune responses and cytokine production.
  • Lipopolysaccharide (LPS) from gram-negative bacteria triggers immune responses via Toll-like receptor 4 (TLR4).
  • Schwann cells (SCs) at injury sites can produce tumor necrosis factor-alpha (TNF-alpha), but mechanisms are unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms of MAPK activation and TNF-alpha gene expression in cultured SCs stimulated by LPS.
  • To clarify the role of CD14 and TLR4 in SC responses to LPS.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) to measure TNF-alpha synthesis.
  • Confocal microscopy to detect intracellular TNF-alpha.
  • Inhibitors (PD98059, SB202190, SP600125) to block MAPK pathways (ERK, p38, JNK).
  • RT-PCR to examine CD14 and TLR4 expression.

Main Results:

  • LPS treatment increased TNF-alpha synthesis in a dose- and time-dependent manner.
  • LPS activated ERK1/2, p38, and SAPK/JNK, indicated by increased phosphorylation.
  • Inhibiting ERK, p38, or JNK pathways significantly reduced LPS-induced TNF-alpha production.
  • CD14 and TLR4 expression were essential for SCs' response to LPS.

Conclusions:

  • LPS stimulates TNF-alpha production in SCs through MAPK signaling pathways (ERK, p38, JNK).
  • The expression of CD14 and TLR4 is critical for SCs to respond to LPS.
  • This study elucidates novel mechanisms of SC response to LPS via MAPK pathways.

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