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Exosomes derived from T regulatory cells relieve inflammatory bowel disease by transferring miR ‐195a‐3p
Author(s) -
Liao Fei,
Lu Xiaohong,
Dong Weiguo
Publication year - 2020
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2385
Subject(s) - microvesicles , inflammatory bowel disease , apoptosis , in vivo , in vitro , spleen , immunology , peripheral blood mononuclear cell , cancer research , microrna , chemistry , biology , medicine , disease , gene , biochemistry , microbiology and biotechnology , pathology
Previous studies have demonstrated the therapeutic effects of regulatory T (Treg) cells on inflammatory bowel disease (IBD), but the mechanism is not well‐understood. Exosomes have been proposed as a novel mechanism underlying the action of Tregs. This study aimed to investigate the therapeutic effects of exosomes secreted by Treg cells (Treg‐Exo) on IBD and to explore the underlying mechanism. Treg‐Exo was isolated from BALB/c mouse spleen mononuclear cells and then injected into a murine model of IBD induced by dextran sodium sulfate (DSS) exposure. A co‐culture model of Treg‐Exo and colonic epithelial YAMC cells in the presence of TNF‐α was used to investigate the communication between Tregs and intestinal epithelial cells. in vitro results showed that Treg‐Exo could be transferred to YAMC cells where Treg‐Exo promoted cell proliferation and inhibited cell apoptosis. Animal experiments showed that Treg‐Exo administration alleviated the DSS‐induced IBD in mice. The therapeutic effects of Treg‐Exo both in vitro and in vivo were eliminated when miR‐195a‐3p expression was inhibited in Treg‐Exo. The pro‐apoptotic Caspase 12 was identified as a direct target of miR‐195a‐3p. In conclusion, Treg‐Exo alleviated the DSS‐induced IBD through transferring miR‐195a‐3p.