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Citrobacter rodentium  is a murine pathogen that serves as a model for enteropathogenic  Escherichia coli. C. rodentium  infection reduced the quantity and activity of mitochondrial respiratory complexes I and IV, as well as phosphorylation capacity, mitochondrial transmembrane potential and ATP generation at day 10, 14 and 19 post infection. Cytokine mRNA quantification showed increased levels of IFN γ , TNF α , IL-4, IL-6, and IL-12 during infection. The effects of adding these cytokines,  C. rodentium  and  E. coli  were hence elucidated using an  in vitro  colonic mucosa. Both infection and TNF α , individually and combined with IFN γ , decreased complex I and IV enzyme levels and mitochondrial function. However, IL-4 reversed these effects, and IL-6 protected against loss of complex IV. Both  in vivo  and  in vitro , the dysfunction appeared caused by nitric oxide-generation, and was alleviated by an antioxidant targeting mitochondria. IFN γ  −/− mice, containing a similar pathogen burden but higher IL-4 and IL-6, displayed no loss of any of the four complexes. Thus, the cytokine environment appears to be a more important determinant of mitochondrial function than direct actions of the pathogen. As IFN γ  and TNF α  levels increase during clearance of infection, the concomitant increase in IL-4 and IL-6 protects mitochondrial function.

IL-4 Protects the Mitochondria Against TNFα and IFNγ Induced Insult During Clearance of Infection with Citrobacter rodentium and Escherichia coli