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Updated: Aug 17, 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

Selective activation of p38 mitogen-activated protein kinase cascade in human neutrophils stimulated by IL-1beta

K Suzuki1, M Hino, H Kutsuna

  • 1Department of Physiology, Osaka City University Medical School, Osaka, Japan.

Journal of Immunology (Baltimore, Md. : 1950)
|November 8, 2001
PubMed

Insights

Interleukin-1beta selectively activates the p38 MAPK pathway in neutrophils, mediating superoxide release and cell adhesion molecule upregulation. This pathway works independently of the ERK pathway in neutrophil activation.

Area of Science:

  • Immunology
  • Cell Signaling
  • Molecular Biology

Background:

  • Interleukin-1beta (IL-1beta) is a key inflammatory cytokine.
  • Mitogen-activated protein kinase (MAPK) pathways are crucial in cellular responses.
  • Neutrophil activation plays a vital role in innate immunity.

Purpose of the Study:

  • To investigate the activation of MAPK cascades in human neutrophils by IL-1beta.
  • To determine the role of p38 MAPK in IL-1beta-induced neutrophil responses.

Main Methods:

  • Stimulation of human neutrophils and endothelial cells with IL-1beta.
  • Assessment of MAPK phosphorylation (p38 MAPK, ERK, JNK) and activation.
  • Measurement of superoxide (O(2)(-)) release, CD11b and CD15 upregulation.
  • Use of SB203580 (p38 MAPK inhibitor) and G-CSF (ERK activator).

Main Results:

  • IL-1beta selectively phosphorylated and activated p38 MAPK and MKK3/6 in neutrophils.
  • IL-1beta induced O(2)(-) release and upregulation of CD11b and CD15, mediated by p38 MAPK.
  • IL-1beta also induced phosphorylation of ERK and JNK in endothelial cells, but only faint ERK phosphorylation in neutrophils.
  • The IL-1beta-p38 MAPK and G-CSF-ERK pathways operate independently in neutrophil activation.

Conclusions:

  • The MKK3/6-p38 MAPK cascade is selectively activated by IL-1beta in human neutrophils.
  • p38 MAPK activation is essential for IL-1beta-induced O(2)(-) release and CD11b/CD15 upregulation.
  • Distinct signaling pathways (IL-1R-p38 MAPK and G-CSF receptor-ERK) independently regulate neutrophil activation.

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