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The forgotten role of lymphangitis in Crohn’s disease

H J Van Kruiningen¹, Jean-Frédéric Colombel²

¹ Department of Pathobiology and Veterinary Science, University of Connecticut, Storrs, Connecticut, USA
² Department of Hepatogastroenterology, Centre Hospitalier Régional, Universitaire de Lille, Lille, France

Correspondence to:
Dr H J Van Kruiningen, Department of Pathobiology and Veterinary Science, University of Connecticut, U-3089, 61 North Eagleville Road, Storrs, CT 06269-3089, USA; Herbert.vankruiningen{at}uconn.edu

Research into Crohn’s 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’s disease occurs in regional lymphatics of the intestine—the 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’s disease, including lymphocytic and granulomatous lymphangitis of the bowel wall and enteroenteric and enterocutaneous fistulas. In Crohn’s 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’s 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.

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