Science and Research

Resolvin E1 Improves Mitochondrial Function in Human Alveolar Epithelial Cells during Severe Inflammation

Severe inflammatory disorders such as sepsis are a major cause of morbidity and mortality worldwide. Mitochondrial dysfunction is regarded as a key feature involved in inflammation pathogenesis. In the present study, we investigated the impact of the omega-3 fatty acid-derived lipid mediator Resolvin E1 (RvE1) on mitochondrial function in experimental pulmonary inflammation. RvE1 was found to exert anti-inflammatory properties in human alveolar epithelial cells during severe inflammation. RvE1 is capable of restoring inflammation-induced mitochondrial dysfunction and the impaired imbalance of mitochondrial fission and fusion. Experimental inhibition of mitochondrial fission with Mdivi-1 in our model is associated with a significantly reduced inflammatory response and improved mitochondrial function. These findings suggest a novel functional mechanism for the beneficial effects of RvE1 in experimental pulmonary inflammatory reactions.

  • Mayer, K.
  • Sommer, N.
  • Hache, K.
  • Hecker, A.
  • Reiche, S.
  • Schneck, E.
  • Weissmann, N.
  • Seeger, W.
  • Hecker, M.

Keywords

  • A549 Cells
  • Alveolar Epithelial Cells/*drug effects/*metabolism
  • Apoptosis/drug effects
  • Eicosapentaenoic Acid/*analogs & derivatives/pharmacology
  • Humans
  • Inflammation/*metabolism
  • Mitochondria/*drug effects
  • *Fission
  • *Fusion
  • *Inflammation
  • *Lung
  • *Mitochondria
  • *Resolvin
Publication details
DOI: 10.1002/lipd.12119
Journal: Lipids
Pages: 53-65 
Number: 1
Work Type: Original
Location: UGMLC
Disease Area: PALI
Partner / Member: JLU
Access-Number: 30697748
See publication on PubMed

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