{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T05:17:13Z","timestamp":1775711833615,"version":"3.50.1"},"reference-count":27,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2005,11,23]],"date-time":"2005-11-23T00:00:00Z","timestamp":1132704000000},"content-version":"vor","delay-in-days":3523,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1996,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>There is now increasing evidence that hyperresponsiveness towards intestinal flora is a crucial event in the pathogenesis of inflammatory bowel disease (IBD). In support of this hypothesis, we recently described in humans that tolerance exists towards indigenous intestinal flora but is broken in active IBD lesions. In the present study, we have attempted to transfer this model into mice from different genetic backgrounds (BALB\/c, SJL\/J, C3H\/HeJ). We found that mononuclear cells from spleen, small bowel and large bowel of mice do not proliferate, <jats:italic>i.e.<\/jats:italic> are tolerant when exposed to bacterial sonicates derived from autologous intestine (BsA) but do proliferate, <jats:italic>i.e.<\/jats:italic> are immune when exposed to bacterial sonicates derived from the heterologous intestine of syngenic littermates (BsH). Furthermore, we demonstrate that both local and systemic tolerance to BsA is broken in a murine model of chronic intestinal inflammation induced by the hapten reagent 2,4,6\u2010trinitrobenzene sulfonic acid (TNBS), which mimics several important characteristics of Crohn's disease. Tolerance to BsA was restored and TNBS\u2010induced colitis was abrogated in mice systemically treated with interleukin (IL)\u201010 or antibodies to IL\u201012. Treatment specifically restored tolerance to BsA, but did not suppress proliferation to BsH. In summary, we here report a new mouse model for the study of immunity and tolerance towards bacterial products. Our data suggest that tolerance to BsA is an important protective mechanism and that restoration of tolerance to resident intestinal flora by IL\u201010 and antibodies to IL\u201012 may be of potential therapeutic utility in patients with inflammatory bowel disease.<\/jats:p>","DOI":"10.1002\/eji.1830260432","type":"journal-article","created":{"date-parts":[[2007,3,2]],"date-time":"2007-03-02T01:49:11Z","timestamp":1172800151000},"page":"934-938","source":"Crossref","is-referenced-by-count":277,"title":["Tolerance towards resident intestinal flora in mice is abrogated in experimental colitis and restored by treatment with interleukin\u201010 or antibodies to interleukin\u201012"],"prefix":"10.1002","volume":"26","author":[{"given":"Rainer","family":"Duchmann","sequence":"first","affiliation":[]},{"given":"Edgar","family":"Schmitt","sequence":"additional","affiliation":[]},{"given":"Percy","family":"Knolle","sequence":"additional","affiliation":[]},{"given":"Karl\u2010Hermann Meyer","family":"Zum B\u00fcschenfelde","sequence":"additional","affiliation":[]},{"given":"Markus","family":"Neurath","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2005,11,23]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/0016-5085(84)90606-1"},{"key":"e_1_2_1_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/0167-5699(87)90853-X"},{"key":"e_1_2_1_4_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2249.1995.tb03836.x"},{"key":"e_1_2_1_5_2","first-page":"175","volume-title":"Inflammatory Bowel Disease: Pathophysiology as Basis of Treatment.","author":"Sartor R. 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