Oxidized lipid species instigate distinct pro- and anti-inflammatory pathways

Oxidized lipids play a critical role in a variety of diseases with two faces: Pro- and anti-inflammatory. However, the molecular mechanisms of this Janus-faced activity remain largely unknown. A recent publication by the Kopf group (IMHS) shed light on the underlying mechanism.

Graphical abstract Muri Kopf
Whereas low concentrations of oxidized lipid species instigate Nrf2-dependent anti-inflammatory responses, high concentrations after TLR priming trigger inflammatory apoptosis and caspase-8-dependent IL-1β processing.

How oxidized lipids regulate inflammatory responses is largely controversial. Investigation by Jonathan Muri et al now revealed that cyclopentenone-containing isoprostanoids such as 15d-PGJ2 possess a dual and opposing bioactivity in inflammation depending on their concentration. Exposure of DCs/macrophages to low concentrations of such lipids before TLR stimulation instigates an anti-inflammatory response mediated by Nrf2-dependent inhibition of NF-kB activation and downstream targets. By contrast, high concentrations of such lipids upon TLR activation of DCs/macrophages result in inflammatory apoptosis characterized by mitochondrial depolarization and caspase-8-mediated IL-1β maturation independently of Nrf2 and the classical inflammasome pathway. These results uncover an unexpected pro- and anti-inflammatory activity of physiologically relevant lipid species generated by enzymatic and non-enzymatic oxidation dependent on their concentration, a phenomenon known as hormesis.  

Link to the paper in Cell Reports.

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