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. 2017 Sep 20;8:1168. doi: 10.3389/fimmu.2017.01168

Table 2.

Inflammasome components and intestinal inflammation.

Mutant strain Trigger Effect Reference
Inflammasome components

Asc−/− DSS Increased pathology (33, 42, 52, 131, 164)
Decreased IL-18 levels (33, 52)
Decreased AMP levels
Treatment with taurine rIL-18 ameliorated disease
(32)

C. rod Increased bacterial colonization (34, 43, 103)
Increased pathology (43, 103)
Decreased IL-18 levels (43)
Decreased mucus secretion by goblet cells (34)

Rotavirus Increased viral load (37)

Casp1−/−Casp11−/− DSS Increased pathology (33, 51, 52, 164)
Decreased IL-18 levels
Phenotype rescued by rIL-18
(51, 52)

C. rod Increased bacterial colonization (34)

FlaTox Decreased IEC pyroptosis (24)

NSAID-induced SI damage Decreased pathology
Decreased IL-1β levels
(165)

Caspase1−/− DSS Decreased pathology
Decreased IL-18 levels
(142)

Rotavirus Increased viral load (37)

Casp1ΔIEC DSS Decreased pathology
Decreased IL-18 levels
(142)

Casp1ΔIEC Rotavirus Increased viral load (37)

Caspase11−/− DSS Increased pathology (47, 48)
Increased IL-18 (48)
Decreased IL-18 and IL-22
Phenotype rescued by rIL-18
(47)

S. Tm Decreased IL-18 levels
Decreased pathology
Increased intraepithelial bacterial burden
Decreased IEC extrusion
(44)

gasdermin D−/− FlaTox Decreased IEC pyroptosis (24)

gasdermin D−/− Rotavirus Increased viral load
Decreased IEC death
(37)

Casp1−/−Casp8−/−Ripk3−/− S. Tm
FlaTox
Decreased IEC extrusion (24)

NLR proteins

NAIP1–6Δ/Δ S. Tm Increased intraepithelial bacterial loads
Decreased IEC expulsion
(14)

NAIP1–6Δ/ΔIEC S. Tm Increased intraepithelial bacterial loads (14)

NLRC4−/− DSS Increased pathology (30)

C. rod Increased bacterial colonization
Increased pathology
Decreased IL-18 at steady state
(25)

S. Tm Increased intraepithelial bacterial loads (14)

iNLRC4+Vil-Cre+ S. Tm
FlaTox
Comparable bacterial burden
Comparable IL-18 and PGE2 levels
Comparable caspase-1 and caspase-8 activation
(24)

NLRP1−/− DSS Increased pathology
Rescued by treatment with rIL-1β or rIL-18 or antibiotics
(131)

NLRP3−/− DSS Increased pathology (30, 42, 52, 164)
Decreased pathology
Decreased IL-1β
(166)

C. rod Increased pathology (43, 103)
Increased bacterial colonization (43, 103)

T cell transfer colitis Increased pathology upon transfer of NLRP3−/− T cells into lymphopenic hosts
Increased Th17 cells and decreased Th1 cells
(167)

NSAID-induced SI damage Decreased pathology
Decreased IL-1β levels
(165)

NLRP6−/− DSS Increased pathology (33)
Decreased IL-18 levels (32, 33)
Decreased AMP levels (32)

C. rod Increased bacterial colonization
Decreased mucus secretion by goblet cells
Decreased autophagosome formation
(34)

NLRP9b−/− Rotavirus Increased viral load
Decreased IEC death
(37)

NLRP9bΔIEC Rotavirus Increased viral load (37)

NLRP12−/− DSS Increased pathology (168170)

NLRX1ΔIEC DSS No change in pathology
Increased IEC proliferation
(40)

PYHIN sensors

AIM2−/− DSS Increased pathology (42, 129)
Decreased IL-1β levels (129)
Decreased IL-18 levels (42, 129)
Decreased IL-22BP levels (42)
Dysregulated AMP levels (42, 129)

AMP, antimicrobial peptides; C. rod, Citrobacter rodentium; FlaTox, Legionella pneumophila flagellin fused to the N-terminal domain of Bacillus anthracis lethal factor; NAIP5, ligand delivered to cytosol; IEC, intestinal epithelial cells; NSAID, non-steroidal anti-inflammatory drugs; SI, small intestine; S. Tm, Salmonella Typhimurium; DSS, dextran sodium sulfate; rIL-18, recombinant IL-18; NLR, NOD-like receptor.

Mutant strain: Casp1ΔIEC, caspase-1-deficient IEC; NAIP1–6Δ/ΔIEC, NAIP1–6-deficient IEC; iNLRC4+Vil-Cre+, NLRC4 only expressed in IEC; NLRP9ΔIEC, NLRP9b-deficient IEC; NLRX1ΔIEC, NLRX1-deficient IEC.