Reference : Unsaturated fatty acids prevent activation of NLRP3 inflammasome in human monocytes/m...
Scientific journals : Article
Human health sciences : Endocrinology, metabolism & nutrition
http://hdl.handle.net/2268/157490
Unsaturated fatty acids prevent activation of NLRP3 inflammasome in human monocytes/macrophages
English
[fr] Les acides gras insaturés préviennent l'activation de l'inflammasome NLRP3 dans les monocytes/macrophages humains
L'Homme, Laurent mailto [Université de Liège - ULiège > > GIGA-R : Virologie - Immunologie >]
Esser, Nathalie mailto [Université de Liège - ULiège > > GIGA-R : Virologie - Immunologie >]
Riva, Laura mailto [Université de Liège - ULiège > > GIGA-R : Virologie - Immunologie >]
Scheen, André mailto [Université de Liège - ULiège > Département des sciences cliniques > Diabétologie, nutrition et maladie métaboliques >]
Paquot, Nicolas mailto [Université de Liège - ULiège > Département des sciences de la santé publique > Nutrition >]
Piette, Jacques mailto [Université de Liège - ULiège > Département des sciences de la vie > GIGA-R : Virologie - Immunologie >]
Legrand, Sylvie mailto [Université de Liège - ULiège > > GIGA-R : Virologie - Immunologie >]
Nov-2013
Journal of Lipid Research
Federation of American Societies for Experimental Biology
54
2998-3008
Yes (verified by ORBi)
International
0022-2275
1539-7262
Bethesda
MD
[en] Fatty acids ; NLRP3 ; Inflammasome ; Obesity ; Diabetes ; Interleukin-1 beta
[en] The NLRP3 inflammasome is involved in many obesity-associated diseases such as type 2 diabetes, atherosclerosis and gouty arthritis through its ability to induce 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 to 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 MSU. UFAs did not affect the transcriptional effect of SFAs suggesting a specific effect on the NLRP3 activation. These results provide a new antiinflammatory mechanism of UFAs by preventing the activation of the NLRP3 inflammasome and therefore the IL-1β processing. By this way, UFAs might play a protective role in NLRP3-associated diseases.
This research has been funded by the Interuniversity Attraction Poles (IAP) program initiated by the Belgian Science Policy Office (BELSPO) (IAP grant P7/32)
http://hdl.handle.net/2268/157490
10.1194/jlr.M037861

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