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TLR2 signals triggered by mycoplasmal lipoprotein/lipopeptide induce K+ efflux to activate the NLRP3 inflammasome

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Title: TLR2 signals triggered by mycoplasmal lipoprotein/lipopeptide induce K+ efflux to activate the NLRP3 inflammasome
Authors: Saeki, Ayumi Browse this author
Into, Takeshi Browse this author
Kataoka, Hideo Browse this author
Hasebe, Akira Browse this author
Shibata, Ken-ichiro Browse this author
Keywords: Toll like receptor 2
mycoplasmal lipoprotein
NLRP3 inflammasome
Issue Date: 15-Sep-2021
Publisher: 北海道歯学会
Journal Title: 北海道歯学雑誌
Volume: 42
Start Page: 52
End Page: 57
Abstract: The proinflammatory cytokine interleukin (IL)- 1β plays a crucial role in controlling bacterial infections and is produced after the processing of pro-IL- 1β by caspase-1, which is activated by the inflammasome. Mycoplasmal membrane lipoprotein and lipopeptide, which are typical Toll-like receptor 2 (TLR2) ligands, activate the NLRP3 inflammasome to produce IL-1β in macrophages, although the molecular mechanism behind this remains unclear. Here, we found that lipoproteins from Mycoplasma salivarium (MsLP) and M. pneumoniae (MpLP) and an M. salivarium-derived lipopeptide (FSL-1) exhibited IL-1β-inducing activity toward bone marrow-derived macrophages from C57BL/6 mice (TLR2+/+ BMMs), whereas the activity toward BMMs from TLR2-deficient mice (TLR2-/- BMMs) was markedly reduced. Microarray analysis suggested that FSL-1 upregulates the potassium voltage-gated channel, subfamily F, member 1 (Kcnf1), which is involved in K+ efflux as one of the NLRP3 inflammasome activators, in a TLR2-dependent manner. Moreover, we found that a high extracellular concentration of K+, which blocks K+ efflux, downregulated the release of IL-1β. Thus, this study is the first to suggest that TLR2-mediated signals triggered by mycoplasmal lipoproteins/lipopeptide upregulate potassium channels to promote K+ efflux, by which the NLRP3 inflammasome is activated.
Type: article
Appears in Collections:北海道歯学雑誌 > 第42巻

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