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  • Unsaturated fatty acids prevent activation of NLRP3 inflammasome in human monocytes/macrophages.

Unsaturated fatty acids prevent activation of NLRP3 inflammasome in human monocytes/macrophages.

Journal of lipid research (2013-09-06)
Laurent L'homme, Nathalie Esser, Laura Riva, André Scheen, Nicolas Paquot, Jacques Piette, Sylvie Legrand-Poels
ABSTRACT

The NLRP3 inflammasome is involved in many obesity-associated diseases, such as type 2 diabetes, atherosclerosis, and gouty arthritis, through its ability to induce interleukin (IL)-1β release. The molecular link between obesity and inflammasome activation is still unclear, but free fatty acids have been proposed as one triggering event. Here we reported opposite effects of saturated fatty acids (SFAs) compared with unsaturated fatty acids (UFAs) on NLRP3 inflammasome in human monocytes/macrophages. Palmitate and stearate, both SFAs, triggered IL-1β secretion in a caspase-1/ASC/NLRP3-dependent pathway. Unlike SFAs, the UFAs oleate and linoleate did not lead to IL-1β secretion. In addition, they totally prevented the IL-1β release induced by SFAs and, with less efficiency, by a broad range of NLRP3 inducers, including nigericin, alum, and monosodium urate. UFAs did not affect the transcriptional effect of SFAs, suggesting a specific effect on the NLRP3 activation. These results provide a new anti-inflammatory mechanism of UFAs by preventing the activation of the NLRP3 inflammasome and, therefore, IL-1β processing. By this way, UFAs might play a protective role in NLRP3-associated diseases.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Palmitic acid, ≥99%
Sigma-Aldrich
Linoleic acid, ≥99%
Sigma-Aldrich
Anti-NLRP3 antibody produced in rabbit, Prestige Antibodies® Powered by Atlas Antibodies, affinity isolated antibody, buffered aqueous glycerol solution
Sigma-Aldrich
Stearic acid, Grade I, ≥98.5% (capillary GC)
Sigma-Aldrich
Oleic acid, ≥99% (GC)