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.
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.
The overall objective of the present study was to evaluate the anti-inflammatory action of a sesquiterpene lactone diacethylpiptocarphol (DPC) from Vernonia scorpioides (Lam.)Pers. and parthenolide (PTH) in Balb-c mice with DSS-induced colitis.
Olive oil activated the IκBα and inhibited NF-κB and cox-2 gene expressions, and p65 nuclear translocation in DSS-colitis mice, reflecting the involvement of the inhibition of NF-κB signaling pathway in the anti-inflammatory olive oil - PPARγ - PGlyRP3 access.
Administration of Dab2-deficient DCs (DC2.4 <sup><i>Dab2</i>-<i>/</i>-</sup> cells) modulated the course of DSScolitis in wild-type mice, enhanced mucosal expression of <i>Tnfa, Il6</i>, and <i>Il17a</i>, and promoted neutrophil recruitment.
Purification of 3, 4-dihydroxyphenylethyl alcohol glycoside from Sargentodoxa cuneata (Oliv.) Rehd. et Wils. and its protective effects against DSS-induced colitis.
The effect of CD1d augmentation and depletion in NOD2-/- mice was assessed in a dextran sodium sulphate [DSS]-induced colitis model via administration of α-GalCer and construction of NOD2-/-CD1d-/- mice.
Age-matched and sex-matched WT (n = 8) and Cld-1 Tg (n = 8) mice were treated with 2.5% DSS in drinking water for 7 days ad libitum (colitis group), followed by drinking water for 10 days (DSS recovery group). b Representative histological images of WT and Cld-1 Tg mice under DSS and DSS recovery protocol showing regenerative crypts in WT DSS Recovery and dysplastic crypts in Cld-1 Tg Recovery. c The mean changes in body weight of the WT and Cld-1 Tg mice after being fed with 2.5% DSS were measured every day until day 7 for the colitis group and day 10 for the DSS recovery group.
Our results indicate that CA could ameliorate DSS-induced colitis through inhibition of NLRP3 inflammasome activation and miR-21 and miR-155 levels in colons and macrophage, suggesting that CA might be a potentially effective drug for UC.
To induce the colitis model, mice continuously consumed water containing 3% DSS for 7 days; some mice were also treated with Sal and the SIRT1/FoxOs pathway blocker selisistat (Ex527).
We found that genetic deletion of CARD9 was sufficient to reduce the development of both spontaneous autoimmune disease as well as DSS- or IL-10 deficiency-associated colitis in <i>Lyn<sup>-/-</sup></i> mice.