{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T19:11:57Z","timestamp":1792264317641,"version":"4.4.0"},"reference-count":46,"publisher":"BMJ","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[2008,1]]},"abstract":"<jats:sec>\n                    <jats:title\/>\n                    <jats:p>Research into Crohn\u2019s disease has recently been focused on the genetics of the patient, the gastrointestinal flora, the gut epithelium and mucosal immune responses. For over 60 years pathologists have reported that the fundamental alteration in Crohn\u2019s disease occurs in regional lymphatics of the intestine\u2014the disease is a lymphocytic and granulomatous lymphangitis. At an earlier time, experimental sclerosis of regional intestinal lymphatics of the pig produced a chronic segmental enteritis with many features of Crohn\u2019s disease, including lymphocytic and granulomatous lymphangitis of the bowel wall and enteroenteric and enterocutaneous fistulas. In Crohn\u2019s disease, differences in the anatomic distribution of vasa recta appear to explain long-segment disease of the ileum and short-segment disease of the more proximal intestine. A variety of bacteria and viruses cause lymphangitis, suggesting that microorganisms may be at the centre of the basic changes in Crohn\u2019s disease. Dietary antigens and lipids are worthy of consideration as well. Now that antibodies to label lymphatics are available, attention should be directed at defining the initial damage to lymphatic endothelium and agents that might be responsible.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1136\/gut.2007.123166","type":"journal-article","created":{"date-parts":[[2007,12,19]],"date-time":"2007-12-19T12:58:09Z","timestamp":1198069089000},"page":"1.1-4","source":"Crossref","is-referenced-by-count":111,"title":["The forgotten role of lymphangitis in Crohn\u2019s disease"],"prefix":"10.1136","volume":"57","author":[{"given":"H J","family":"Van Kruiningen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Fr\u00e9d\u00e9ric","family":"Colombel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"239","published-online":{"date-parts":[[2007,12,19]]},"reference":[{"key":"2025121307401127000_57.1.1.1","doi-asserted-by":"crossref","first-page":"475","DOI":"10.1016\/S0889-8553(21)00207-7","article-title":"Current concepts of the etiology and pathogenesis of ulcerative colitis and Crohn\u2019s disease.","volume":"24","author":"Sartor","year":"1995","journal-title":"Gastroenterol Clin North Am"},{"key":"2025121307401127000_57.1.1.2","first-page":"215","article-title":"Inflammatory bowel disease. 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