IL-22 promotes occludin expression by activating autophagy and treats ulcerative colitis
IL-22 serves a protective function in the intestinal barrier. These protective properties of IL-22 may offer a potential treatment for ulcerative colitis (UC). However, the exact mechanisms of action remain unclear. Autophagy plays an important protective role in stabilizing the intestinal barrier....
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| Veröffentlicht in: | Molecular and cellular biochemistry 2024-06, Vol.479 (6), p.1443-1450 |
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| creator | Nong, Hui Yuan, Haifeng Lin, Yiting Chen, Siyu Li, Yanbo Luo, Zhaoqiong Yang, Wen Zhang, Tao Chen, Yuanneng |
| description | IL-22 serves a protective function in the intestinal barrier. These protective properties of IL-22 may offer a potential treatment for ulcerative colitis (UC). However, the exact mechanisms of action remain unclear. Autophagy plays an important protective role in stabilizing the intestinal barrier. We aimed to explore the role of autophagy in the IL-22-mediated-protective effects in UC. Dextran sulfate sodium (DSS) was administrated via drinking water over 7 days to induce acute UC in BALB/c mice. Treatments with IL-22 (0.25 μg/10 g bodyweight) were started by intraperitoneal injection on days 1, 3, and 5. Weight, disease activity index, histological score, and myeloperoxidase (MPO) activity were used to evaluate the severity of colitis. The expressions of occludin and autophagy-related proteins LC3BII/I were measured by western blot analysis. The lipopolysaccharide-induced HT-29 cell model was used to explore the mechanism. In vivo, IL-22 significantly alleviated DSS-induced clinical manifestations, reduced histological injury, and inhibited MPO activity. IL-22 upregulated the expression of occludin and the LC3B II/I ratio in the colon. In vitro, IL-22 significantly lowered TNF-α levels and enhanced the expression of occludin and the LC3B II/I ratio. Importantly, inhibiting autophagy in vitro by 3-Methyladenine (3-MA) attenuated the occludin protective effects of IL-22. In summary, our findings demonstrate that IL-22 ameliorates DSS-induced ulcerative colitis, which may be attributable to activating autophagy and then promoting occludin expression. |
| doi_str_mv | 10.1007/s11010-023-04806-z |
| format | Article |
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These protective properties of IL-22 may offer a potential treatment for ulcerative colitis (UC). However, the exact mechanisms of action remain unclear. Autophagy plays an important protective role in stabilizing the intestinal barrier. We aimed to explore the role of autophagy in the IL-22-mediated-protective effects in UC. Dextran sulfate sodium (DSS) was administrated via drinking water over 7 days to induce acute UC in BALB/c mice. Treatments with IL-22 (0.25 μg/10 g bodyweight) were started by intraperitoneal injection on days 1, 3, and 5. Weight, disease activity index, histological score, and myeloperoxidase (MPO) activity were used to evaluate the severity of colitis. The expressions of occludin and autophagy-related proteins LC3BII/I were measured by western blot analysis. The lipopolysaccharide-induced HT-29 cell model was used to explore the mechanism. In vivo, IL-22 significantly alleviated DSS-induced clinical manifestations, reduced histological injury, and inhibited MPO activity. IL-22 upregulated the expression of occludin and the LC3B II/I ratio in the colon. In vitro, IL-22 significantly lowered TNF-α levels and enhanced the expression of occludin and the LC3B II/I ratio. Importantly, inhibiting autophagy in vitro by 3-Methyladenine (3-MA) attenuated the occludin protective effects of IL-22. In summary, our findings demonstrate that IL-22 ameliorates DSS-induced ulcerative colitis, which may be attributable to activating autophagy and then promoting occludin expression.</description><identifier>ISSN: 0300-8177</identifier><identifier>ISSN: 1573-4919</identifier><identifier>EISSN: 1573-4919</identifier><identifier>DOI: 10.1007/s11010-023-04806-z</identifier><identifier>PMID: 37440121</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Autophagy ; Autophagy - drug effects ; Biochemistry ; Biomedical and Life Sciences ; Cancer Research ; Cardiology ; Colitis, Ulcerative - chemically induced ; Colitis, Ulcerative - drug therapy ; Colitis, Ulcerative - metabolism ; Colitis, Ulcerative - pathology ; Dextran ; Dextran sulfate ; Dextran Sulfate - toxicity ; Dextrans ; Drinking water ; Gene Expression Regulation - drug effects ; HT29 Cells ; Humans ; Inflammatory bowel disease ; Interleukin 22 ; Interleukins - metabolism ; Intestine ; Life Sciences ; Lipopolysaccharides ; Male ; Medical Biochemistry ; Mice ; Mice, Inbred BALB C ; Microtubule-Associated Proteins - metabolism ; Occludin - metabolism ; Peroxidase ; Tumor necrosis factor-α ; Ulcerative colitis</subject><ispartof>Molecular and cellular biochemistry, 2024-06, Vol.479 (6), p.1443-1450</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. 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The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-aadb2350b42b2b528f507742e11a8dab80c391a33977d6cc7ebf61fd3a993b843</citedby><cites>FETCH-LOGICAL-c375t-aadb2350b42b2b528f507742e11a8dab80c391a33977d6cc7ebf61fd3a993b843</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11010-023-04806-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11010-023-04806-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37440121$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nong, Hui</creatorcontrib><creatorcontrib>Yuan, Haifeng</creatorcontrib><creatorcontrib>Lin, Yiting</creatorcontrib><creatorcontrib>Chen, Siyu</creatorcontrib><creatorcontrib>Li, Yanbo</creatorcontrib><creatorcontrib>Luo, Zhaoqiong</creatorcontrib><creatorcontrib>Yang, Wen</creatorcontrib><creatorcontrib>Zhang, Tao</creatorcontrib><creatorcontrib>Chen, Yuanneng</creatorcontrib><title>IL-22 promotes occludin expression by activating autophagy and treats ulcerative colitis</title><title>Molecular and cellular biochemistry</title><addtitle>Mol Cell Biochem</addtitle><addtitle>Mol Cell Biochem</addtitle><description>IL-22 serves a protective function in the intestinal barrier. These protective properties of IL-22 may offer a potential treatment for ulcerative colitis (UC). However, the exact mechanisms of action remain unclear. Autophagy plays an important protective role in stabilizing the intestinal barrier. We aimed to explore the role of autophagy in the IL-22-mediated-protective effects in UC. Dextran sulfate sodium (DSS) was administrated via drinking water over 7 days to induce acute UC in BALB/c mice. Treatments with IL-22 (0.25 μg/10 g bodyweight) were started by intraperitoneal injection on days 1, 3, and 5. Weight, disease activity index, histological score, and myeloperoxidase (MPO) activity were used to evaluate the severity of colitis. The expressions of occludin and autophagy-related proteins LC3BII/I were measured by western blot analysis. The lipopolysaccharide-induced HT-29 cell model was used to explore the mechanism. In vivo, IL-22 significantly alleviated DSS-induced clinical manifestations, reduced histological injury, and inhibited MPO activity. IL-22 upregulated the expression of occludin and the LC3B II/I ratio in the colon. In vitro, IL-22 significantly lowered TNF-α levels and enhanced the expression of occludin and the LC3B II/I ratio. Importantly, inhibiting autophagy in vitro by 3-Methyladenine (3-MA) attenuated the occludin protective effects of IL-22. In summary, our findings demonstrate that IL-22 ameliorates DSS-induced ulcerative colitis, which may be attributable to activating autophagy and then promoting occludin expression.</description><subject>Animals</subject><subject>Autophagy</subject><subject>Autophagy - drug effects</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cancer Research</subject><subject>Cardiology</subject><subject>Colitis, Ulcerative - chemically induced</subject><subject>Colitis, Ulcerative - drug therapy</subject><subject>Colitis, Ulcerative - metabolism</subject><subject>Colitis, Ulcerative - pathology</subject><subject>Dextran</subject><subject>Dextran sulfate</subject><subject>Dextran Sulfate - toxicity</subject><subject>Dextrans</subject><subject>Drinking water</subject><subject>Gene Expression Regulation - drug effects</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Inflammatory bowel disease</subject><subject>Interleukin 22</subject><subject>Interleukins - metabolism</subject><subject>Intestine</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Medical Biochemistry</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microtubule-Associated Proteins - metabolism</subject><subject>Occludin - metabolism</subject><subject>Peroxidase</subject><subject>Tumor necrosis factor-α</subject><subject>Ulcerative colitis</subject><issn>0300-8177</issn><issn>1573-4919</issn><issn>1573-4919</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P3DAQhi1UxC4ff6CHylIvvbjM2EnsHCtEC9JKXEDiZtmOs80qG29tBwG_HtOFVuqhp5E8z7wzfgj5iPAVAeR5QgQEBlwwqBQ07PmALLGWglUtth_IEgQAUyjlghyntIFCA-IRWQhZVYAcl-T-esU4p7sYtiH7RINz49wNE_WPu-hTGsJE7RM1Lg8PJg_Tmpo5h91Psy6PU0dz9CYnOo_Ox9J_8NSFcchDOiWHvRmTP3urJ-Tu--XtxRVb3fy4vvi2Yk7IOjNjOstFDbbiltuaq74GKSvuEY3qjFXgRItGiFbKrnFOets32HfCtK2wqhIn5Ms-t3zh1-xT1tshOT-OZvJhTpor0ShZyaYu6Od_0E2Y41Su0wJkLVVbIxaK7ykXQ0rR93oXh62JTxpBv3rXe--6eNe_vevnMvTpLXq2W9_9GXkXXQCxB1JpTWsf_-7-T-wLCyeONQ</recordid><startdate>20240601</startdate><enddate>20240601</enddate><creator>Nong, Hui</creator><creator>Yuan, Haifeng</creator><creator>Lin, Yiting</creator><creator>Chen, Siyu</creator><creator>Li, Yanbo</creator><creator>Luo, Zhaoqiong</creator><creator>Yang, Wen</creator><creator>Zhang, Tao</creator><creator>Chen, Yuanneng</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20240601</creationdate><title>IL-22 promotes occludin expression by activating autophagy and treats ulcerative colitis</title><author>Nong, Hui ; 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These protective properties of IL-22 may offer a potential treatment for ulcerative colitis (UC). However, the exact mechanisms of action remain unclear. Autophagy plays an important protective role in stabilizing the intestinal barrier. We aimed to explore the role of autophagy in the IL-22-mediated-protective effects in UC. Dextran sulfate sodium (DSS) was administrated via drinking water over 7 days to induce acute UC in BALB/c mice. Treatments with IL-22 (0.25 μg/10 g bodyweight) were started by intraperitoneal injection on days 1, 3, and 5. Weight, disease activity index, histological score, and myeloperoxidase (MPO) activity were used to evaluate the severity of colitis. The expressions of occludin and autophagy-related proteins LC3BII/I were measured by western blot analysis. The lipopolysaccharide-induced HT-29 cell model was used to explore the mechanism. In vivo, IL-22 significantly alleviated DSS-induced clinical manifestations, reduced histological injury, and inhibited MPO activity. IL-22 upregulated the expression of occludin and the LC3B II/I ratio in the colon. In vitro, IL-22 significantly lowered TNF-α levels and enhanced the expression of occludin and the LC3B II/I ratio. Importantly, inhibiting autophagy in vitro by 3-Methyladenine (3-MA) attenuated the occludin protective effects of IL-22. In summary, our findings demonstrate that IL-22 ameliorates DSS-induced ulcerative colitis, which may be attributable to activating autophagy and then promoting occludin expression.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37440121</pmid><doi>10.1007/s11010-023-04806-z</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Autophagy Autophagy - drug effects Biochemistry Biomedical and Life Sciences Cancer Research Cardiology Colitis, Ulcerative - chemically induced Colitis, Ulcerative - drug therapy Colitis, Ulcerative - metabolism Colitis, Ulcerative - pathology Dextran Dextran sulfate Dextran Sulfate - toxicity Dextrans Drinking water Gene Expression Regulation - drug effects HT29 Cells Humans Inflammatory bowel disease Interleukin 22 Interleukins - metabolism Intestine Life Sciences Lipopolysaccharides Male Medical Biochemistry Mice Mice, Inbred BALB C Microtubule-Associated Proteins - metabolism Occludin - metabolism Peroxidase Tumor necrosis factor-α Ulcerative colitis |
| title | IL-22 promotes occludin expression by activating autophagy and treats ulcerative colitis |
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