Cutting edge: critical role for mesothelial cells in necrosis-induced inflammation through the recognition of IL-1 alpha released from dying cells

J Immunol. 2008 Dec 15;181(12):8194-8. doi: 10.4049/jimmunol.181.12.8194.

Abstract

Endogenous danger signals released from necrotic cells are thought to be sensed by phagocytes leading to secretion of IL-1alpha and neutrophilic recruitment. However, the mechanisms for IL-1alpha production and IL-1alpha-mediated sterile inflammation remain poorly understood. We report here that necrotic cell extracts elicited little secretion of CXCL1 and IL-6 from macrophages but robust production in mesothelial cells. The induction of CXCL1 as well as activation of NF-kappaB and MAPKs by cytosolic extracts required the presence of IL-1alpha in the necrotic cell. Conversely, expression of IL-1R and MyD88 but not IL-1alpha, RICK, TLR2, TLR4, TRIF, or inflammasome components in mesothelial cells was critical for the production of CXCL1. Furthermore, IL-1alpha was critical to induce the recruitment of neutrophils in the peritoneal cavity via CXCR2. These studies show that IL-1alpha is a key danger signal released from necrotic cells to trigger CXCL1 secretion and recruitment of neutrophils via IL-1R/MyD88 on neighboring mesothelial cells.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chemokine CXCL1 / metabolism
  • Cytosol / immunology
  • Cytosol / metabolism
  • Cytosol / pathology
  • Epithelium / immunology*
  • Epithelium / metabolism
  • Epithelium / pathology*
  • Inflammation Mediators / metabolism
  • Inflammation Mediators / physiology*
  • Interleukin-1alpha / deficiency
  • Interleukin-1alpha / genetics
  • Interleukin-1alpha / metabolism*
  • Interleukin-6 / metabolism
  • Liver / cytology
  • Liver / immunology
  • Macrophages, Peritoneal / immunology
  • Macrophages, Peritoneal / metabolism
  • Macrophages, Peritoneal / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Necrosis
  • Neutrophil Infiltration / immunology
  • Peritoneal Cavity / pathology

Substances

  • Chemokine CXCL1
  • Inflammation Mediators
  • Interleukin-1alpha
  • Interleukin-6