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IL-4 Protects the Mitochondria Against TNF alpha and IFN gamma Induced Insult During Clearance of Infection with Citrobacter rodentium and Escherichia coli

Artikel i vetenskaplig tidskrift
Författare Arpan K. Maiti
Sinan Sharba
Nazanin Navabi
Huamei Forsman
Harvey Robert Fernandez
Sara K. Lindén
Publicerad i Scientific Reports
Volym 5
Sidor Article nr. 15434
ISSN 2045-2322
Publiceringsår 2015
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor Article nr. 15434
Språk en
Länkar dx.doi.org/10.1038/srep15434
Ämnesord tumor-necrosis-factor, murine colonic hyperplasia, pro-inflammatory, cytokines, interferon-gamma, cell-death, respiratory-chain, epithelial-cells, up-regulation, in-vivo, apoptosis
Ämneskategorier Cellbiologi

Sammanfattning

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 gamma, TNF alpha, 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 alpha, individually and combined with IFN gamma, 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 gamma -/- 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 gamma and TNF alpha levels increase during clearance of infection, the concomitant increase in IL-4 and IL-6 protects mitochondrial function.

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