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Intestinal permeability to translocation of bacterial products is increased in cirrhosis. Regulatory T cells (Tregs) remain central to the interplay between the host and microbial milieu. We propose that Tregs are involved in promoting gut barrier integrity and a balanced interaction with gut microbiota–derived short‐chain fatty acids (SCFAs). Carbon tetrachloride cirrhosis was induced in wild‐type and recombination activating gene 1 ( Rag1 ) ‐/‐  mice. Naive T cells and Treg cells were transferred into  Rag1  ‐/‐  mice. Intestinal permeability was assessed  in vivo  after lipopolysaccharide (LPS) oral administration, and bacterial DNA presence was evaluated in mesenteric lymph nodes. Transcript and protein levels of tight‐junction (TJ) proteins were measured in colonic tissue. Intestinal T helper profile in response to  Escherichia coli  ( E. coli ) was determined by flow cytometry. SCFAs were measured by gas chromatography–mass spectrometry in colonic content before and after  E. coli  challenge.  Rag1  ‐/‐  mice showed significantly increased permeability to LPS and bacterial DNA translocation rate compared with control mice. Naive T and Treg cotransfer significantly reduced gut permeability to bacterial antigen translocation and restored TJ protein expression in  Rag1  ‐/‐  mice. Naive T and Treg replenishment in  Rag1  ‐/‐  mice restrained proinflammatory differentiation of intestinal lymphocytes in response to  E. coli . The main SCFA concentration resulted in significant reduction in  Rag1  ‐/‐  mice after  E. coli  administration but remained unaltered after naive T and Tregs cotransfer. The reduced expression of SCFA receptors induced by  E. coli  was reestablished following naive T and Treg reconstitution in  Rag1  ‐/‐  mice.  Conclusion:  The restriction of gut permeability, local inflammatory differentiation, and loss of bacteria‐derived SCFAs foster the value of Tregs in preventing bacterial translocation in cirrhosis.

Regulatory T Cells Restrict Permeability to Bacterial Antigen Translocation and Preserve Short‐Chain Fatty Acids in Experimental Cirrhosis