Aims. Diabetes is a proinflammatory state, evidenced by increased pattern recognition receptors and the inflammasome\n(NOD-like receptor family pyrin domain (NLRP)) complex. Recent reports have elucidated the role of the gut microbiome\nin diabetes, but there is limited data on the gut microbiome in NLRP-KO mice and its effect on diabetes-induced\ninflammation. Methods. Gut microbiome composition and biomarkers of inflammation (IL-18, serum amyloid A) were\nassessed in streptozotocin- (STZ-) induced diabetic mice on a NLRP3-knockout (KO) background versus wild-type diabetic\nmice. Results. SAA and IL-18 levels were significantly elevated in diabetic mice (STZ) compared to control (WT) mice,\nand there was a significant attenuation of inflammation in diabetic NLRP3-KO mice (NLRP3-KO STZ) compared to\ncontrol mice (p < 0 005). Principal coordinate analysis clearly separated controls, STZ, and NLRP3-KO STZ mice. Among\nthe different phyla, there was a significant increase in the Firmicutes : Bacteroidetes ratio in the diabetic group compared to\ncontrols. When compared to the WT STZ group, the NLRP3-KO STZ group showed a significant decrease in the\nFirmicutes : Bacteroidetes ratio. Together, these findings indicate that interaction of the intestinal microbes with the innate\nimmune system is a crucial factor that could modify diabetes and complications.
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