Journal of applied microbiology · 2026
Latilactobacillus curvatus K4G4 suppresses NLRP3 inflammasome activation via IL-10 induction and ameliorates monosodium urate-induced peritonitis.
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Yamada Kazuha, Okano Aki, Tanaka Sachi, Takase Ryuichi, Watanabe Jun
Аннотация
AIMS: This study aimed to determine whether heat-killed Latilactobacillus curvatus K4G4 exerts anti-inflammatory effects in vivo using a monosodium urate-induced peritonitis mouse model, and to elucidate the underlying mechanisms with a focus on IL-10-mediated regulation of NLRP3 inflammasome activation in macrophages.
METHODS AND RESULTS: C57BL/6 J mice were fed K4G4-supplemented diets for 2 weeks prior to monosodium urate challenge. K4G4 significantly reduced monosodium urate-induced neutrophil infiltration and suppressed the expression of Il1b and Nlrp3 in peritoneal cells. Spleen IL-10 levels were elevated in K4G4-fed mice. In J774.1 cells, K4G4 pretreatment increased Il10 expression and IL-10 secretion, and dose-dependently inhibited LPS/nigericin-induced IL-1β production and LDH release. IL-10 neutralization restored IL-1β production, indicating IL-10-dependent suppression of inflammasome activation. K4G4 also inhibited the priming step by reducing LPS-induced Il1b, Tnfa, and Nlrp3 transcription and suppressing NF-κB nuclear translocation. Furthermore, K4G4 attenuated LPS/nigericin-induced caspase-1 activation, confirming inhibition of the activation step.
CONCLUSIONS: Heat-killed K4G4 suppresses MSU-induced peritonitis in vivo and is associated with inhibition of both the priming and activation steps of NLRP3 inflammasome signaling, potentially involving IL-10-dependent mechanisms.
METHODS AND RESULTS: C57BL/6 J mice were fed K4G4-supplemented diets for 2 weeks prior to monosodium urate challenge. K4G4 significantly reduced monosodium urate-induced neutrophil infiltration and suppressed the expression of Il1b and Nlrp3 in peritoneal cells. Spleen IL-10 levels were elevated in K4G4-fed mice. In J774.1 cells, K4G4 pretreatment increased Il10 expression and IL-10 secretion, and dose-dependently inhibited LPS/nigericin-induced IL-1β production and LDH release. IL-10 neutralization restored IL-1β production, indicating IL-10-dependent suppression of inflammasome activation. K4G4 also inhibited the priming step by reducing LPS-induced Il1b, Tnfa, and Nlrp3 transcription and suppressing NF-κB nuclear translocation. Furthermore, K4G4 attenuated LPS/nigericin-induced caspase-1 activation, confirming inhibition of the activation step.
CONCLUSIONS: Heat-killed K4G4 suppresses MSU-induced peritonitis in vivo and is associated with inhibition of both the priming and activation steps of NLRP3 inflammasome signaling, potentially involving IL-10-dependent mechanisms.