Published online Aug 15, 2013. doi: 10.4291/wjgp.v4.i3.63
Revised: June 8, 2013
Accepted: June 19, 2013
Published online: August 15, 2013
It has been a big puzzle as why the inflammation of ulcerative colitis (UC) is limited to the mucosa, while in Crohn’s disease (CD) the inflammation is transmural and can be seen in all layers of the gut. Here, I give a tentative explanation extended from the unified hypothesis I proposed on the etiology of inflammatory bowel disease. This hypothesis suggested that both UC and CD are caused by weakening of the gut barrier due to damage of the protective mucus layer and the underlying tissue by the poorly inactivated digestive proteases resulting from a reduction of gut bacteria by dietary chemicals like saccharin and sucralose. However, the large amounts of bacteria in the colon make the recruitment of neutrophils and formation of crypt abscess the main manifestation of UC, while the infiltration of antigens and dietary particles in the small and large intestine mainly cause the recruitment of macrophages and formation of granulomas as the main manifestations in CD. The fast reacting and short life span of neutrophils make the fight and damage limited to the surface of the mucosa. In contrast, the long life span and constant movement of macrophages may bring the harmful agents deep into the tissue. Therefore, the pathogenesis of UC may be more like bacterial pneumonia, while CD may be more like pneumoconiosis or tuberculosis of the lung.
Core tip: In my opinion, ulcerative colitis is more like bacterial pneumonia with the involvement of mainly neutrophils, capacious exudates into the cavity but limited damage of the tissue, while Crohn’s disease is more like pneumoconiosis, such as silicosis or berylliosis, or tuberculosis of the lung with the involvement of mainly macrophages and manifested as granulomatous inflammation in the interstices, destruction of the tissue, extensive proliferation of fibroblasts and formation of fibrosis.