Lung and Intestine: A Specific Link in an Ulcerative Colitis Rat Model

Figure 7

Possible microvasculature mechanism on how colitis affects lungs in the immune-TNBS-ethanol-induced UC rat model, perhaps related to the common ancestry of the bowel and the bronchial tree. Some etiological factors like smoke exposure may lead to gut-originating T-cell mishoming and promoting growth of enteric bacteria in the lung during inflammatory responses. Systemic IL-6, in conjunction with localized TGF-β, may drive cross-organ Th17-polarized inflammation. Systemic IL-13 may drive aberrant NKT and macrophage responses across organs. Inflammation triggers a change in the endothelium of the intestinal and pulmonary vasculature leading to increased adhesion molecule expression, platelet activation, angiogenesis, and coagulation with decreased endothelial barrier functions.