The Effect of Rebamipide on Cellular Release of Leukotriene B4 by Helicobacter Pylori. Jung Jin Lee 1 ’ Bok Gee Han 2 ’ Jai Youl Ro 3 ’ K1vang Ho Rhee 4 ， Hee Shang YollIl 4 ’ Mal Nam Kim 1 ’ and Myung Hee Chung 5 lDepartment of Biology， Sangmyung University; 2Division of Degenerative Disease， National Institute of Health; 3Department of Pharmacology， College of Medicine， Yonsei University; 4Department of Microbiology， College of Medicine， Gyeongsang National University; and 5Department of Pharmacology， College of Medicine， Seoul National University， Seoul 110-799， Korea Leukotrienes(LTs) are known to act as a mediator provoking tissue r‘esponse in inflammation. This finding implicates that LTs also play important roles in the pathogenesis of H. pylori-induced gastritis and gastric ulceration. Rebamipide is being currently used as a therapeutics for gastritis and peptic ulcer， but their mechanisms of action have not been known clearly yet. One possibility is that their therapeutic effects are ascribed to interfering with the H. pylori-induced release of LTs from neutrophils and gastric mucosal cells. In the present study， this possibility was tested using LTB4 as the test material in human neutrophils and Kato III cells(gastric adenoma cells as a substitute for gastric mucosal cells). The release of LTB4 from both neutrophils and Kato III cells was time and H. pylori-dose dependent. The maximum release of LTB4 was induced by neutrophils and Kato III cells when these cells incubated with H. pylori 4.8 X 108 cellsjml for 30min. But in the presence of rebamipide the release of LTB4 from these cells was suppressed in dose dependent manners. The release was completely suppressed at 1.0 mM of rebamipide in neutrophils and 2.0 mM of this drug in Kato III cells， respectively. We also obtained the resu1ts that the release of LTB4 was induced by A23187(Ca