Inflammatory Bowel Disease: Treatment Modalities and Mucosal Prostaglandin/Leukotriene Formation
Ulcerative colitis (UC) and Crohn’s disease are inflammatory diseases of unknown etiology. Not only are the etiologies unknown, but the soluble mediators that amplify and modulate the inflammatory response have not been fully explored. Our studies have focused on delineating the soluble mediators of inflammation in inflammatory bowel disease (IBD) with emphasis on the role played by arachidonic acid metabolitis via the cyclooxygenase pathway, prostaglandin E2 (PGE2), thromboxane A2 (TXA2), prostacyclin I2 (PGI2), and the lipoxygenase product leukotriene B4 (LTB4) and 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE). Some early events in inflammation, such as vascular dilatation and increased vascular permeability with gaps between vascular endothelial cells, are common to all organ systems. Monocytes and neutrophils adhere to the surface of venule endothelial cells and subsequently migrate from the bloodstream into injured tissue through the process of diapedesis.
KeywordsInflammatory Bowel Disease Arachidonic Acid Ulcerative Colitis Colonic Mucosa Ulcerative Colitis Patient
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