Cell Biochemistry and Biophysics

, Volume 44, Issue 2, pp 179–186

Preserved coupling of oxidative phosphorylation but decreased mitochondrial respiratory capacity in IL-1β-treated human peritoneal mesothelial cells

Authors

  • Sylvia Stadlmann
    • Department of Pathological AnatomyUniversity Hospital Innsbruck
  • Kathrin Renner
    • Department of PathophysiologyInnsbruck Medical University
  • Juergen Pollheimer
    • Institute of Ecology and Conservation BiologyUniversity of Vienna
  • Patrizia Lucia Moser
    • Department of Pathological AnatomyUniversity Hospital Innsbruck
  • Alain Gustave Zeimet
    • Department of Obstetrics and GynecologyUniversity Hospital Innsbruck
  • Felix Albert Offner
    • Department of PathologyAcademic Teaching Hospital Feldkirch
    • Department of General and Transplant Surgery, D. Swarovsky Research LaboratoryInnsbruck Medical University
Original Article

DOI: 10.1385/CBB:44:2:179

Cite this article as:
Stadlmann, S., Renner, K., Pollheimer, J. et al. Cell Biochem Biophys (2006) 44: 179. doi:10.1385/CBB:44:2:179
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Abstract

The peritoneal mesothelium acts as a regulator of serosal responses to injury, infection, and neoplastic diseases. After inflammation of the serosal surfaces, proinflammatory cytokines induce an “activated” mesothelial cell phenotype, the mitochondrial aspect of which has not previously been studied. After incubation of cultured human peritoneal mesothelial cells with interleukin (IL)-1β for 48 h, respiratory activity of suspended cells was analyzed by high-resolution respirometry. Citrate synthase (CS) and lactate dehydrogenase (LDH) activities were determined by spectrophotometry. Treatment with IL-1β resulted in a significant decline of respiratory capacity (p<0.05). Respiratory control ratios (i.e., uncoupled respiration at optimum carbonyl cyanide p-trifluoromethoxyphenylhydrazone concentration divided by oligomycin inhibited respiration measured in unpermeabilized cells) remained as high as 11, indicating well-coupled mitochondria and functional integrity of the inner mitochondrial membrane. Whereas respiratory capacities of the cells declined in proportion with decreased CS activity (p<0.05), LDH activity increased (p<0.05). Taken together, these results indicate that IL-1β exposure of peritoneal mesothelial cells does not lead to irreversible defects or inhibition of specific components of the respiratory chain, but is associated with a decrease of mitochondrial content of the cells that is correlated with an increase in LDH (and thus glycolytic) capacity.

Index Entries

Peritoneal mesothelial cellsinterleukin-1β, mitochondria, respiration, citrate synthase, lactate dehydrogenasecell viability
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Copyright information

© Humana Press Inc. 2006