{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["McNamee EN"],"funding":["NIDDK NIH HHS","NIAID NIH HHS"],"pagination":["16711-6"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3189085"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["108(40)"],"pubmed_abstract":["IL-37, a newly described member of the IL-1 family, functions as a fundamental inhibitor of innate inflammation and immunity. In the present study, we examined a role for IL-37 during experimental colitis. A transgenic mouse strain was generated to express human IL-37 (hIL-37tg), and these mice were subjected to dextran sulfate sodium (DSS)-induced colitis. Despite the presence of a CMV promoter to drive expression of IL-37, mRNA transcripts were not present in colons at the resting state. Expression was observed only upon disruption of the epithelial barrier, with a six- to sevenfold increase (P = 0.02) on days 3 and 5 after continuous exposure to DSS. During the development of colitis, clinical disease scores were reduced by 50% (P < 0.001), and histological indices of colitis were one-third less in hIL-37tg mice compared with WT counterparts (P < 0.001). Reduced inflammation was associated with decreased leukocyte recruitment into the colonic lamina propria. In addition, release of IL-1β and TNFα from ex vivo colonic explant tissue was decreased 5- and 13-fold, respectively, compared with WT (P ≤ 0.005), whereas IL-10 was increased sixfold (P < 0.001). However, IL-10 was not required for the anti-inflammatory effects of IL-37 because IL-10-receptor antibody blockade did not reverse IL-37-mediated protection. Mechanistically, IL-37 originating from hematopoietic cells was sufficient to exert anti-inflammatory effects because WT mice reconstituted with hIL-37tg bone marrow were protected from colitis. Thus, IL-37 emerges as key modulator of intestinal inflammation."],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Interleukin 37 expression protects mice from colitis."],"pmcid":["PMC3189085"],"funding_grant_id":["R01 DK080212","DK080212","R01 AI015614","R56 AI015614","AI15614"],"pubmed_authors":["Jedlicka P","Bufler P","Grenz A","Rivera-Nieves J","McNamee EN","Masterson JC","Collins CB","McManus M","Nold MF","Nold-Petry C","Dinarello CA"],"additional_accession":[]},"is_claimable":false,"name":"Interleukin 37 expression protects mice from colitis.","description":"IL-37, a newly described member of the IL-1 family, functions as a fundamental inhibitor of innate inflammation and immunity. In the present study, we examined a role for IL-37 during experimental colitis. A transgenic mouse strain was generated to express human IL-37 (hIL-37tg), and these mice were subjected to dextran sulfate sodium (DSS)-induced colitis. Despite the presence of a CMV promoter to drive expression of IL-37, mRNA transcripts were not present in colons at the resting state. Expression was observed only upon disruption of the epithelial barrier, with a six- to sevenfold increase (P = 0.02) on days 3 and 5 after continuous exposure to DSS. During the development of colitis, clinical disease scores were reduced by 50% (P < 0.001), and histological indices of colitis were one-third less in hIL-37tg mice compared with WT counterparts (P < 0.001). Reduced inflammation was associated with decreased leukocyte recruitment into the colonic lamina propria. In addition, release of IL-1β and TNFα from ex vivo colonic explant tissue was decreased 5- and 13-fold, respectively, compared with WT (P ≤ 0.005), whereas IL-10 was increased sixfold (P < 0.001). However, IL-10 was not required for the anti-inflammatory effects of IL-37 because IL-10-receptor antibody blockade did not reverse IL-37-mediated protection. Mechanistically, IL-37 originating from hematopoietic cells was sufficient to exert anti-inflammatory effects because WT mice reconstituted with hIL-37tg bone marrow were protected from colitis. Thus, IL-37 emerges as key modulator of intestinal inflammation.","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Oct","modification":"2025-07-05T03:05:23.681Z","creation":"2025-07-05T03:05:23.681Z"},"accession":"S-EPMC3189085","cross_references":{"pubmed":["21873195"],"doi":["10.1073/pnas.1111982108"]}}