Utilizing the AOM-DSS model, mice with a myeloid-specific deletion of Egfr had significantly decreased tumor multiplicity and burden, protection from high-grade dysplasia and significantly reduced colitis.
Here we demonstrate that LIGHT signaling through LTβR, rather than HVEM, plays a critical role in the progression of DSS-induced colitis, as LTβR deficient mice exhibit a more severe disease phenotype.
Il1rl2<sup>-/-</sup> mice and mice given injections of an antibody against IL36R developed less severe colitis and fibrosis after administration of DSS or TNBS, but bone marrow cells from Il1rl2<sup>-/-</sup> mice did not prevent induction of colitis and fibrosis.
Cell-specificity studies using cre-lox mice demonstrate that the loss of NLRX1 in intestinal epithelial cells (IEC) recapitulate the increased sensitivity to DSScolitis observed in whole body <i>Nlrx1</i><sup>-/-</sup> mice.
In the present study, we have explored the therapeutic effect of a RAL family protein of filarial parasite Wuchereria bancrofti i.e., rWbL2 protein against DSS induced colitis in a mouse model.
Consequently, one compound, namely DI-1 was selected and its therapeutic activity evaluated using mouse models of experimental colitis (induced by TNBS and DSS).
In consistence with these results, COMMD10-deficiency in Ly6C<sup>hi</sup> monocytes, but not in intestinal-resident lamina propria macrophages, led to increased IL-1β production and aggravated colonic inflammation in a model of DSS-induced colitis.
Here we utilized photoconvertible KikGR mice to track immune cells from the caecum and ascending (proximal) colon in the steady state and DSS-induced colitis.
To investigate the alleviative effect of a ropy-exopolysaccharide (EPS) producing strain, Bifidobacterium longum subsp. longum YS108R, on experimental colitis, C57BL/6J mice (male, 6-8 weeks old) were randomly assigned to six groups (n = 8): normal control, DSS colitis and four DSScolitis groups orally administered with three B. longum subsp. longum strains (YS108R, C11A10B and HAN4-25) and B. animalis subsp. lactis BB12, respectively, in which YS108R produced ropy-EPS, C11A10B produced non-ropy-EPS, HAN4-25 did not produce EPS and BB12 was set as a positive control.
Compared with the DSS model group, the expression of Kv1.3, iNOS, NLRP3, ASC, caspase-1p20, pro-IL-1β and IL-1β in colon were decreased in the DSS-induced colitis mice with PAP-1 injection.
Similarly, the protective effect of PGE₂ on indomethacin-induced small intestinal damage or DSS-induced colitis was mimicked by EP3/EP4 agonists or EP4 agonists, respectively.