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Furthermore, SFA-derived crystals provoked acute inflammation, which was impaired in IL-1β-deficient mice. I'm currently working on Namco's LAN environmental entertainment called 'LEDZONE' (Though I'm actually not an employee of Namco). Excess SFAs also induced crystallization and IL-1β release in vivo. Indeed, SFA-derived crystals activated NLRP3 inflammasome and subsequent IL-1β release via lysosomal dysfunction. These results suggest that SFAs activate NLRP3 inflammasome through intracellular crystallization. As well as IL-1β release, the intracellular crystallization and lysosomal dysfunction were inhibited in the presence of oleic acid. Analyses using polarized light microscopy revealed that intracellular crystallization was provoked in SFA-treated macrophages. The treatment with SFAs, such as palmitic acid and stearic acid, promoted IL-1β release in murine primary macrophages while treatment with oleic acid inhibited SFA-induced IL-1β release in a dose-dependent manner.

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Therefore, we investigated the underlying mechanism by which SFAs trigger NLRP3 inflammasome activation. Total Audio Converter 5.2.74 Serial Koumei Satou K.s. Recent investigations suggest the possible role of the NLRP3 (nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain containing 3) inflammasome, which regulates IL-1β (interleukin 1β) release and leads to inflammation, in this process. Inflammation provoked by the imbalance of fatty acid composition, such as excess saturated fatty acids (SFAs), is implicated in the development of metabolic diseases. Kasahara, M.T.) and Division of Biophysics, Department of Physiology (A.S.-T., N.S.), Jichi Medical University, Tochigi, Japan Department of Internal Medicine (Endocrinology and Metabolism), Faculty of Medicine, University of Tsukuba, Ibaraki, Japan (T.M., H.S.) Graduate School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan (H.T.) and Drug Design Laboratory, Graduate School of Medical Life Science, Yokohama City University, Kanagawa, Japan (S.-Y.P.).

2 From the Division of Inflammation Research, Center for Molecular Medicine (T. 1 From the Division of Inflammation Research, Center for Molecular Medicine (T.

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