Response of human peritoneal mesothelial cells to inflammatory injury is regulated by interleukin-1beta and tumor necrosis factor-alpha

Wound Repair Regen. Mar-Apr 2006;14(2):187-94. doi: 10.1111/j.1743-6109.2006.00109.x.


Peritoneal injury is often associated with alterations of the mesothelium, resulting in peritoneal healing and adhesion formation. We analyzed the effects of pro-inflammatory cytokines on cell morphology and proliferation of human peritoneal mesothelial cells (HPMC). After 48 hours, HPMC formed a confluent layer with cell volumes of 2,662+/-111 fL. Treatment of HPMC with interleukin-1beta and tumor necrosis factor-alpha (TNF-alpha) induced mesothelial disintegration and alterations in mesothelial cell morphology, which were associated with an interleukin-1beta-triggered increase in cell volume (3,028+/-118 fL; p<0.05) and exfoliation of cells into the supernatants of cell cultures (p<0.05). Whereas TNF-alpha arrested HPMC in the G0/G1 phase (p<0.05), interleukin-1beta caused an increase of cells into the S phase of the cell cycle. In addition, interleukin-1beta and interferon-gamma exerted a proliferative effect on HPMC. These changes were independent from mesothelial Na+/H+ antiporter-1 expression. Our data indicate that the response of HPMC to inflammatory injury is regulated by interleukin-1beta and TNF-alpha reflecting their putative role in peritoneal wound healing and adhesion formation.

MeSH terms

  • Blotting, Western
  • Cell Adhesion Molecules / drug effects
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Epithelium / drug effects*
  • Epithelium / ultrastructure
  • Flow Cytometry
  • Humans
  • Integrins / drug effects
  • Interleukin-1 / pharmacology*
  • Microscopy, Electron, Scanning
  • Peritoneum / cytology
  • Peritoneum / drug effects*
  • Peritoneum / ultrastructure*
  • Time Factors
  • Tumor Necrosis Factor-alpha / pharmacology*


  • Cell Adhesion Molecules
  • Integrins
  • Interleukin-1
  • Tumor Necrosis Factor-alpha