Table 1.

Summary of current pre-clinical evidence supporting the differential role of NLRP3 inflammasome in intestinal inflammation.

Animal model	Genetic phenotype	Treatment/timing	Outcome	Role of NLRP3	Reference
DSS	Nlrp3−/−, Asc−/−, and caspase-1−/−	2.5% (w/v)/6 days	✓ Body weight loss ✓ Diarrhea ✓ Rectal bleeding mortality	Protective	(7)
TNBS	Nlrp3−/−, Asc−/−, and caspase-1−/−	(30 mg/mL)/3 days	✓ Body weight loss ✓ Diarrhea ✓ Rectal bleeding mortality	Protective	(7)
DSS	Nlrp3−/−, Asc−/−, and caspase-1−/−	✓ 3% (w/v)/5 days and sacrifice at day 7 ✓ 3% (w/v)/7 days and sacrifice at day 9	✓ Disruption of the intestinal epithelial barrier ✓ Increase in mucosal permeability ✓ Bacterial translocation ✓ Systemic dissemination	Protective	(37)
DSS	Nlrp3−/−, Asc−/−, caspase-1−/−	2% (w/v)/9 days	✓ Less severity of colitis ✓ Reduced pro-inflammatory cytokines levels	Detrimental	(9)
DSS	Nlrp3−/−, Asc−/−, caspase-1−/−	2% (w/v)/9 days	✓ Less severity of colitis ✓ Reduced pro-inflammatory cytokines levels	Detrimental	(41)
IL-10−/−	IL-10−/−	n.a.	✓ Increase in colonic IL-1β and IL-17 levels	Detrimental	(42)

DSS, dextran sodium sulfate; TNBS, 2,4,6-trinitrobenzenesulfonic acid; w/v, weight/volume; IL-1β, interleukin-1beta; IL-17, interleukin-17.