{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,26]],"date-time":"2026-10-26T20:10:35Z","timestamp":1793045435421,"version":"4.5.0"},"reference-count":59,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2024,5,10]],"date-time":"2024-05-10T00:00:00Z","timestamp":1715299200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>\n                      Inflammatory bowel disease (IBD) is a chronic disease involving multiple genes, and the current available targeted drugs for IBD only deliver moderate efficacy. Whether there is a single gene that systematically regulates IBD is not yet known.\n                      <jats:italic>MiR-146a<\/jats:italic>\n                      plays a pivotal role in repression of innate immunity, but its function in the intestinal inflammation is sort of controversy, and the genetic regulatory networks regulated by miR-146a in IBD has not been revealed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      RT-qPCR was employed to detect the expression of\n                      <jats:italic>miR-146a<\/jats:italic>\n                      in IBD patients and in a mouse IBD model induced by dextran sulfate sodium (DSS), and then we generated a\n                      <jats:italic>miR-146a<\/jats:italic>\n                      knock-out mouse line with C57\/Bl6N background. The disease activity index was scored in DSS-treated miR-146a deficiency mice and their wild type (\n                      <jats:italic>WT<\/jats:italic>\n                      ) littermates. Bulk RNA-sequencing, RT-qPCR and immunostaining were done to illustrate the downstream genetic regulatory networks of\n                      <jats:italic>miR-146a<\/jats:italic>\n                      in flamed colon. Finally, the modified\n                      <jats:italic>miR-146a<\/jats:italic>\n                      mimics were used to treat DSS-induced IBD in\n                      <jats:italic>miR-146a<\/jats:italic>\n                      knock-out and\n                      <jats:italic>WT<\/jats:italic>\n                      IBD mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We showed that the expression of\n                      <jats:italic>miR-146a<\/jats:italic>\n                      in the colon was elevated in dextran sulfate sodium (DSS)-induced IBD mice and patients with IBD. DSS induced dramatic body weight loss and more significant rectal bleeding, shorter colon length, and colitis in\n                      <jats:italic>miR-146a<\/jats:italic>\n                      knock-out mice than\n                      <jats:italic>WT<\/jats:italic>\n                      mice. The miR-146a mimics alleviated DSS-induced symptoms in both\n                      <jats:italic>\n                        miR-146a\n                        <jats:sup>-\/-<\/jats:sup>\n                      <\/jats:italic>\n                      and\n                      <jats:italic>WT<\/jats:italic>\n                      mice. Further RNA sequencing illustrated that the deficiency of\n                      <jats:italic>miR-146a<\/jats:italic>\n                      de-repressed majority of DSS-induced IBD-related genes that cover multiple genetic regulatory networks in IBD, and supplementation with\n                      <jats:italic>miR-146a<\/jats:italic>\n                      mimics inhibited the expression of many IBD-related genes. Quantitative RT-PCR or immunostaining confirmed that\n                      <jats:italic>Ccl3, Saa3, Csf3, Lcn2, Serpine1, Serpine2<\/jats:italic>\n                      , MMP3, MMP8, MMP10, IL1A, IL1B, IL6, CXCL2, CXCL3, S100A8, S100A9, TRAF6, P65, p-P65, and IRAK1 were regulated by miR-146a in DSS induced IBD. Among them,\n                      <jats:italic>MMP3, MMP10, IL6, IL1B, S100A8, S100A9, SERPINE1, CSF3<\/jats:italic>\n                      , and\n                      <jats:italic>IL1A<\/jats:italic>\n                      were involved in the active stage of IBD in humans.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      Our date demonstrated that miR-146a acts as a top regulator in C57\/BL6N mice to systematically repress multiple genetic regulatory networks involved in immune response of intestine to environment factors, and combinatory treatment with\n                      <jats:italic>miR-146a-5p<\/jats:italic>\n                      and\n                      <jats:italic>miR-146a-3p<\/jats:italic>\n                      mimics attenuates DSS-induced IBD in mice through down-regulating multiple genetic regulatory networks which were increased in colon tissue from IBD patients. Our findings suggests that\n                      <jats:italic>miR-146a<\/jats:italic>\n                      is a top inhibitor of IBD, and that\n                      <jats:italic>miR-146a-5p<\/jats:italic>\n                      and\n                      <jats:italic>miR-146a-3p<\/jats:italic>\n                      mimics might be potential drug for IBD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2024.1366319","type":"journal-article","created":{"date-parts":[[2024,5,10]],"date-time":"2024-05-10T00:36:06Z","timestamp":1715301366000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":21,"title":["MiR-146a alleviates inflammatory bowel disease in mice through systematic regulation of multiple genetic 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