We investigated the effects of TiO<sub>2</sub> in the development of colitis and the role of the nucleotide-binding oligomerisation domain receptor, pyrin domain containing (NLRP)3 inflammasome.
We studied the effect of heat-killed cells of <i>E. faecalis</i> on NLRP3 inflammasome activation in THP-1-derived macrophages.Pretreatment of <i>E. faecalis</i> or NLRP3 siRNA can inhibit NLRP3 inflammasome activation in macrophages in response to fecal content or commensal microbes, <i>P. mirabilis</i> or <i>E. coli</i>, according to the reduction of caspase-1 activation and IL-1β maturation.Mechanistically, <i>E. faecalis</i> attenuates the phagocytosis that is required for the full activation of the NLRP3 inflammasome.In in vivo mouse experiments, <i>E. faecalis</i> can ameliorate the severity of intestinal inflammation and thereby protect mice from dextran sodium sulfate (DSS)-induced colitis and the formation of CRC in wild type mice.On the other hand, <i>E. faecalis</i> cannot prevent DSS-induced colitis in NLRP3 knockout mice.
One inflammasome in particular, NLRP3, has been analysed extensively in its contribution to colitis and has been shown to be associated with the development of colitis-associated colorectal cancer.
Nlrp3(-/-) mice showed an increase in acute and recurring colitis and CAC, although the disease outcome was less severe in Nlrp3(-/-) mice than in Pycard(-/-) or Casp1(-/-) animals.
Therefore, we investigated the therapeutic effects of CAI in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rat colitis and the involvement of CAI action with NLRP3 inflammasome and NF-κB pathway.
Here we further investigated the anti-inflammatory effect of compound 1 in DSS-induced colitis in C57BL/6 and NLRP3(-/-) mice, and revealed the possible modulation by compound 1 of NLRP3 inflammasome-mediated IL-1β release from macrophages.
The present study was to investigate the protective effects of curcumin on dextran sulfate sodium (DSS)-induced colitis through inhibiting NLRP3 inflammasome activation and IL-1β production.
In this study, we investigated the anti-inflammatory effect of Huaier in dextran sulfate sodium (DSS)-induced murine colitis and revealed the underlying mechanisms by targeting NLRP3 inflammasomes.
The underlying mechanisms for the protective effect of MALT1 inhibitors in DSS-induced colitis may be attributed to its inhibition on NF-κB and NLRP3 inflammasome activation in macrophages.
Thus, our research describes a mechanism by which KA/GPR35 signaling represses adaptive NLRP3 inflammasome activation to increase colitis susceptibility and suggests a potential metabolic target for the intervention of stress-related colonic disorder.
NLRP3 inflammasome has been reported to be associated with inflammatory bowel disease including colitis due to its potential ability to induce IL-1β secretion.