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- W2912335146 abstract "Abstract Background: Macrophages (Mf) are key in innate immunity and inflammation. Toll-like receptors (TLR) sense bacterial-derived products and trigger the inflammation. Big-conductance (BK) channels contribute to cell repolarization and participate in signal transduction. The role of BKs in innate immunity is largely unknown. Methods: We stimulated RAW246.7 Mf with ligands of pro-inflammatory TLRs (TLR2-PGN, TLR4-LPS or TLR7/8-R848)± BK blocker iberiotoxin or opener NS1619 and analyzed RNA by PCR, protein by ELISA and western blot, DNA-binding by EMSA. Results: TLRs augmented BK RNA and protein levels. Chemical BK block inhibited Mf activation via TLR2, TLR4 and TLR7/8, indicated by reduced production of TNFα, IL-1, IL-6, IL-8 at the levels of both RNA and secreted protein. The inhibitory effect of BK block was time- and dose-dependent and was specific to stimulation with TLR ligands (not observed upon Mf stimulation with TNFα). Upstream in signaling, BK block prevented TLR-induced activation of the transcription factor NFκB in an IκBα-dependent manner. Further, BK block prevented MAPK p38 phosphorylation but spared activation of ERK. In contrast BK opener augmented LPS-induced NFkB activation and TNFα production with minimal effect of MAPK; its effect on TLR2- and TLR7/8-induced Mf activation was minimal. In conclusion, we identified that BK channels are key for TLR-induced pro-inflammatory activation of macrophages and could be useful for the control of TLR/Mf function." @default.
- W2912335146 created "2019-02-21" @default.
- W2912335146 creator A5034826085 @default.
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- W2912335146 date "2010-04-01" @default.
- W2912335146 modified "2023-09-25" @default.
- W2912335146 title "BK channel controls the TLR-induced pro-inflammatory activation of macrophages via IκBα/NFκB and p38 MAPK signaling. (136.35)" @default.
- W2912335146 doi "https://doi.org/10.4049/jimmunol.184.supp.136.35" @default.
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