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Updated: Oct 11, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
09:04

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells

Published on: May 22, 2014

The mitogen-activated protein kinase p38 is necesssary for interleukin 1beta-induced monocyte chemoattractant protein

B H Rovin1, W A Wilmer, M Danne

  • 1Department of Medicine, Division of Nephrology, The Ohio State University, Columbus, OH, USA.

Cytokine
|March 25, 1999
PubMed

Insights

p38 kinase activation is essential for interleukin 1beta (IL-1beta) to induce monocyte chemoattractant protein-1 (MCP-1) expression in human mesangial cells. ERK2 activation does not play a role in this IL-1beta-mediated gene activation.

Area of Science:

  • Cellular and Molecular Biology
  • Immunology
  • Signal Transduction

Background:

  • Mitogen-activated protein (MAP) kinases are implicated in cytokine-induced gene expression.
  • Interleukin 1beta (IL-1beta) is a key inflammatory cytokine.
  • Chemokines like MCP-1 play crucial roles in immune responses.

Purpose of the Study:

  • To investigate the roles of p38 kinase and ERK2 in IL-1beta-induced MCP-1 expression in human mesangial cells.
  • To determine the specific signaling pathways mediating IL-1beta's effects on MCP-1.

Main Methods:

  • Treatment of human mesangial cells with IL-1beta.
  • Assessing p38 and ERK2 activation via phosphorylation and kinase activity assays.
  • Utilizing selective inhibitors SB 203580 (for p38) and PD 098059 (for MEK1).
  • Measuring MCP-1 mRNA and protein levels.
  • Evaluating NF-kappaB activation (nuclear translocation and DNA binding).

Main Results:

  • IL-1beta treatment significantly increased p38 kinase phosphorylation and activity.
  • Inhibition of p38 kinase with SB 203580 reduced IL-1beta-induced MCP-1 mRNA and protein levels.
  • SB 203580 did not affect MCP-1 mRNA stability or IL-1beta-induced NF-kappaB activation.
  • Inhibition of ERK activation with PD 098059 had no impact on IL-1beta-induced MCP-1 expression or NF-kappaB activation.

Conclusions:

  • p38 kinase is a necessary mediator for IL-1beta-induced MCP-1 expression in human mesangial cells.
  • p38 kinase acts downstream of NF-kappaB activation in this pathway.
  • ERK2 does not mediate IL-1beta-induced MCP-1 gene expression in these cells.

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