Inflammatory Bowel DiseaseRichard P. MacDermott, William F. Stenson |
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Page 192
... MEDIATORS PREFORMED HISTAMINE PROTEOGLYCANS TRYPTASE Vasculature increased permeability , edema , endothelial cell proliferation . CHYMASE CHEMOTACTIC FACTORS Epithelium detachment , increased mucus secretion , necrosis LIPID - DERIVED ...
... MEDIATORS PREFORMED HISTAMINE PROTEOGLYCANS TRYPTASE Vasculature increased permeability , edema , endothelial cell proliferation . CHYMASE CHEMOTACTIC FACTORS Epithelium detachment , increased mucus secretion , necrosis LIPID - DERIVED ...
Page 196
... mediators are released by stimuli in the inflamed intestine ? It is clear that some secretagogues induce release of a selected portion of mediators . Although many mast cell products have defined effects in vitro , the net effects of ...
... mediators are released by stimuli in the inflamed intestine ? It is clear that some secretagogues induce release of a selected portion of mediators . Although many mast cell products have defined effects in vitro , the net effects of ...
Page 201
... mediators . Identification of the latter has greatly expanded to include also platelet - activating factor ( PAF ) , biogenic amines , kinins , complement ... mediators of inflammation in IBD and that 201 Chapter 10 Inflammatory Mediators /
... mediators . Identification of the latter has greatly expanded to include also platelet - activating factor ( PAF ) , biogenic amines , kinins , complement ... mediators of inflammation in IBD and that 201 Chapter 10 Inflammatory Mediators /
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abnormalities acid action activity addition agents alterations antibodies antigens appear associated bacterial blood cause chronic Clin clinical colonic compared complement complex component Crohn's disease cytokines cytotoxic decreased defect determined diarrhea effects enhanced epithelial cells epithelium et al evidence expression factor findings function Gastroenterology genes genetic granulomas growth human immune immune response Immunol immunologic important incidence increased induced infection inflammation inflammatory bowel disease inhibition initially injury intestinal involved isolated lamina propria lesions leukocyte levels lymphocytes macrophages markers mast cells mechanisms mediators mononuclear mucin mucosal Nature neutrophils normal observed occur patients population possible potential present production prostaglandin protein rates recent receptor regulation relatives release reported response risk role schistosomiasis secretion secretory serum shown specific stimulation studies suggest T-cell tissue ulcerative colitis vitro