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As outlined above, deconjugation and epimerization of colonic bile acids alters their affinity for transmembrane receptors, which in turn alters their signaling consequences. Examples of this include effects on neuroendocrine signaling in the colon ( 12, 13, 18, 27 ), modification of the host cell content of lipid raft domains ( 12, 18 ), inhibition of colonic epithelial cell proliferation ( 12, 21 ), inhibition of inflammatory signaling ( 20, 24, 45 ), and regulation of secretion ( 26, 30 ). In addition to these direct effects of bile acids on target cells, the modification of the composition of the colonic microbiota also has profound influences on colonic physiology, as discussed in more detail below. Pharmacological targeting of bile acid metabolism has also emerged as a potential therapeutic approach in the treatment of inflammatory bowel disease (IBD) and other colonic disorders. This is based in part on the ability of the principal bile acids, which are conjugated, to effectively seal the intestinal barrier, particularly in their unconjugated form ( 38 ). UDCA is currently the only bile acid conjugate approved for clinical use. It has been shown to have beneficial effects on the intestinal mucosa of IBD patients in clinical trials ( 11, 38, 55 ), and in animal models of colonic diseases ( 13, 27 ). Furthermore, TUDCA, a secondary bile acid, has been shown to have similar if not improved effects as compared to UDCA ( 22 ), and has been incorporated into the management of IBD patients ( 23 ).

Under normal conditions, bile acids undergo a series of metabolic modifications by the resident microbiota in the colon. As deconjugated, unconjugated primary bile acids are predominantly secreted by the liver, the colonic microbiota may play an important role in their metabolism. They can be converted into secondary bile acids via deconjugation, dehydroxylation, and epimerization. A recent study found that specific strains of clostridia in the distal colon of mice metabolized CDCA to increase its hydrophobicity and thus increased its absorption ( 23 ). This study therefore suggests the possibility that a diet high in secondary bile acids could be therapeutically beneficial for IBD patients, and further studies are needed to confirm this possibility.

Ursodeoxycholic acid inhibits mucosal leukocyte trafficking and mucosal production of cytokines in dextran sulfate sodium (DSS)-induced colitis in mice. A randomized, controlled study was performed to determine the effect of ursodeoxycholic acid (UDCA) on intestinal mucosal inflammation in the dextran sulfate sodium (DSS)-induced colitis model in mice. UDCA (20 mg/kg p.o.) was administered daily for 7 days in parallel with DSS induction. Ten days after the initiation of UDCA treatment, mice were sacrificed, and their colons were harvested. The mucosal leukocyte influx and the expression of inflammatory cytokines in the colon tissues were measured by flow cytometric and quantitative real-time PCR analysis, respectively. UDCA treatment prevented infiltration of inflammatory cells in the colitis tissue. The UDCA-treated mice also showed a significant decrease in the expression of colonic inflammatory cytokines, including TNF-α, IFN-γ, and IL-1β, compared to the control group. Additionally, UDCA treatment inhibited the expressions of other cytokines in the inflammatory microenvironment and upregulated the expression of T-bet in the colon tissue. UDCA can also inhibit mucosal production of proinflammatory cytokines in DSS-induced colitis and the effect is mediated by blocking the transport of these cytokines from the blood into the colon tissue. These findings demonstrate that UDCA may have a therapeutic effect on intestinal inflammatory disorders via inhibition of mucosal production of proinflammatory cytokines and mucosal leukocyte trafficking.
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