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.
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.
Furthermore, preemptive dexamethasone treatment of DSS-challenged SAMP mice led to changes in flora composition without preventing the development of colitis.
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.
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.
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.
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.
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).
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.
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.
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.