Mitochondria and redox balance in coeliac disease: A case-control study

Coeliac disease (CD) is a gluten-sensitive autoimmune disorder. Gluten toxicity encompasses a wide spectrum of target organ functions and pathologies, including the activation of the immune response and triggering of oxidative stress. The aim of this study was to investigate inflammation and the redox balance in patients with active CD, and to evaluate whether alteration of mitochondrial function is involved in the disease status.

In this prospective case-control study, blood samples from sixteen adult CD patients and sixteen healthy controls (HC) were investigated for IL-1β, IL-6 and IL-8 plasma concentrations, for serum PON1 arylesterase, total and MnSOD antioxidant enzyme activities, induced TBARs levels, and for lymphocyte mtDNA content.

Patients showed IL-8 and IL-1β concentrations significantly higher than HC counterparts. Patients had a significantly higher content of induced TBARS compared to HC value, indicating a shift in their serum redox balance towards pro-oxidant species. The assay of antioxidant enzyme activities showed a significant 25% increase in PON1, a higher total SOD, and a significant 21% higher MnSOD in patients compared to HC. Lymphocyte mtDNA content in patients was significantly twofold higher than in HC, supporting the induction of mitochondrial biogenesis. The patients' mitochondrial compensatory response may explain the correlation between MnSOD activity and mtDNA content. The patients' mitochondrial oxidative stress, cooperating to cytokines secretion, may justify the correlation between IL-1β concentration and mtDNA content.

These results highlight the mitochondrial involvement in CD and suggest the evaluation of the mtDNA content as a potential diagnostic and follow-up parameter.