Genetic and environmental factors contribute to the etiology of ulcerative colitis and Crohn's disease. Both produce irritable bowel disease (IBD) affecting approximately 1 million patients in the United States. In experimental models of ulcerative colitis, there is enhanced angiogenesis at sites of inflammation leading to increased permeability and thrombogenic potential. In this issue, Tolsanova et al., show that vascular epithelial growth factor (VEGF) has a causative role in angiogenesis leading to experimental ulcerative colitis. The authors injected neutralizing anti-VEGF antibody intramuscularly after disease induction and found decreased colonic lesions, attenuation of the colonic permeability increase, and less inflammatory cells in the colonic mucosa. They also found that the increased VEGF during onset of disease was correlated with activation of the Src kinase and that treatment with a Src inhibitor attenuated the colonic permeability increase. It is concluded that VEGF plays a pathogenic role in ulcerative colitis and that anti-VEGF antibody inhibits this colitis via Src-mediated mechanism. Overall, the results give an insight into the etiology of IBD.
See article at J Pharmacol Exp Ther 2009, 328:749-757.
- The American Society for Pharmacology and Experimental Therapeutics