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Inflammatory bowel disease and lymphology: a discontinuous thread revisited in the molecular era.

In this issue of Lymphology, Becker and colleagues (1) meticulously dissect molecular mechanisms, develop new insights, and review current concepts on the molecular basis, pathophysiologic events, and historical context implicating “lymphatic dysregulation” as a key player in the pathogenesis, defense, and progression of inflammatory bowel disease (IBD). Drawing on the explosion in “molecular lymphology” during the past 15 years, the authors implicate novel regulatory factors and new roles for familiar signaling pathways linked to inflammation-induced lymphatic alterations associated with lymphangiogenesis and tissue remodeling. While their focus is on non-infectious enteritis, IBD spans a spectrum of intestinal disorders, some of which can be traced to specific microbes as etiologic agents and others, perhaps by default, classified as noninfectious immune disorders, i.e., not linked to a specific microbe. Indeed, in their original description in 1932, Crohn et al (2) distinguished cases of regional ileitis among the “benign granulomatous tumors” which clinically and histologically resembled tuberculous enteritis but where the tubercle bacillus could not be isolated or identified on tissue section. From the outset, lymphatic system abnormalities – increased lymphatic vessel density and vigorous immune system response – Lymphology 47 (2014) 1-2