title: Inhibitory effects of catechins on neutrophil-dependent gastric inflammation.
abstract: The inhibitory effects of tea against carcinogenesis have been attributed to the biological activity of the polyphenol fraction of tea. However, the molecular mechanisms of these effects are not completely understood. Chronic inflammation induced by Helicobacterpylori has been proposed to be a causative pathway in the carcinogenesis of stomach cancer. Therefore, an agent possessing anti-inflammatory properties may be chemopreventative against stomach cancer. In the present study, we have investigated the anti-inflammatory effects of tea catechins. After addition of IL-1beta to MKN45 cells, a gastric cancer cell line, or human umbilical vein endothelial cells (HUVECs), IL-8 production was detected in supernatants. This IL-8 production was inhibited by catechins. Incubation of HUVECs or polymorphonuclear leukocytes (PMNs) with IL-1beta or IL-8, respectively, resulted in an increased surface expression of adhesion molecules. Catechins also inhibited this expression of adhesion molecules on HUVECs and PMNs. Of these major effects, the strongest effect of catechins was to reduce expression of the adhesion molecules CD1lb and CD18 on PMNs. These results suggest that tea may inhibit carcinogenesis partly through the anti-inflammatory effects of tea catechins on PMN-dependent gastric mucosal inflammation.
authors.affiliation: First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kawaramachidori Hirokouji Agaru, Kyoto, Japan.
authors.forename: Osamu
authors.initials: O
authors.lastname: Handa
authors.forename: Yuji
authors.initials: Y
authors.lastname: Naito
authors.forename: Tomohisa
authors.initials: T
authors.lastname: Takagi
authors.forename: Takeshi
authors.initials: T
authors.lastname: Ishikawa
authors.forename: Miho
authors.initials: M
authors.lastname: Ueda
authors.forename: Naoyuki
authors.initials: N
authors.lastname: Matsumoto
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kokura
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ichikawa
authors.forename: Norimasa
authors.initials: N
authors.lastname: Yoshida
authors.forename: Kayoko
authors.initials: K
authors.lastname: Shimoi
authors.forename: Toshikazu
authors.initials: T
authors.lastname: Yoshikawa
mesh_terms: D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D039481:CD11b Antigen / Q000096:biosynthesis; D018821:CD18 Antigens / Q000096:biosynthesis; D002392:Catechin / Q000378:metabolism / Q000494:pharmacology*; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000166:cytology; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D006801:Humans; D007249:Inflammation; D007375:Interleukin-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D008297:Male; D009504:Neutrophils / Q000378:metabolism*; D013270:Stomach / Q000276:immunology / Q000473:pathology*; D013662:Tea; D014407:Tumor Cells, Cultured; D014471:Umbilical Veins / Q000166:cytology
chemical_list: D000893:Anti-Inflammatory Agents; D039481:CD11b Antigen; D018821:CD18 Antigens; D007375:Interleukin-1; D016209:Interleukin-8; D013662:Tea; D002392:Catechin