Table 3.

Modulation of the NLRP3 inflammasome by gut microbial derivatives and metabolites.

Derivatives and metabolites of gut microbiota	Modulation of the NLRP3 inflammasome
LPS	Involved in the typical and atypical activation processes of the NLRP3 inflammasome, promoting the release of IL-1β and IL-18.
BAs	BAs are a class of DAMPs that activate NLRP3 inflammasomes in a Ca2+ influx-dependent manner, whereas FXR inhibits NLRP3 inflammasome activity through physical interaction with NLRP3 and caspase-1.
IS	Related studies have confirmed the ability of IS to promote cardiomyocyte apoptosis and fibrosis by upregulating NLRP3 inflammatory vesicle components (NLRP3, ASC, and protease-1).
TMAO	TMAO is associated with the formation and activation of NLRP3 inflammasome. ROS production is the most common pathway in inflammasome assembly. A related study found that TMAO could activate NLRP3 inflammatory vesicles by inhibiting the SIRT3-SOD2-mitochondrial ROS signaling pathway.
SCFA	SCFAs are capable of inducing K+ efflux of the epithelial cell membrane in a GPR43-dependent manner, which has been linked to the activation of the NLRP3 inflammasome. SCFA also contributes significantly to the function of the intestinal barrier, and low levels of SCFAs can lead to a decrease in the engagement of metabolite-sensing G protein-coupled receptors, which can compromise the integrity of the gut and facilitate the entry of substances, such as LPS, into the bloodstream and tissues, which can contribute to the activation of the NLRP3 inflammasome.