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