Original Article

Cell Biochemistry and Biophysics

, Volume 44, Issue 2, pp 179-186

First online:

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

  • Sylvia StadlmannAffiliated withDepartment of Pathological Anatomy, University Hospital Innsbruck
  • , Kathrin RennerAffiliated withDepartment of Pathophysiology, Innsbruck Medical University
  • , Juergen PollheimerAffiliated withInstitute of Ecology and Conservation Biology, University of Vienna
  • , Patrizia Lucia MoserAffiliated withDepartment of Pathological Anatomy, University Hospital Innsbruck
  • , Alain Gustave ZeimetAffiliated withDepartment of Obstetrics and Gynecology, University Hospital Innsbruck
  • , Felix Albert OffnerAffiliated withDepartment of Pathology, Academic Teaching Hospital Feldkirch
  • , Erich GnaigerAffiliated withDepartment of General and Transplant Surgery, D. Swarovsky Research Laboratory, Innsbruck Medical University Email author 

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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 cells interleukin-1β, mitochondria, respiration, citrate synthase, lactate dehydrogenase cell viability