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北海道歯学雑誌 >
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TLR2 signals triggered by mycoplasmal lipoprotein/lipopeptide induce K+ efflux to activate the NLRP3 inflammasome
| 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 | | nterleukin-1β | | mycoplasmal lipoprotein | | FSL-1 | | 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 |
| URI: | http://hdl.handle.net/2115/82757 |
| Appears in Collections: | 北海道歯学雑誌 > 第42巻
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