Gastric epithelial cell CXC chemokine secretion following Helicobacter pylori infection in vitro

被引:25
作者
Sieveking, D
Mitchell, HM
Day, AS [1 ]
机构
[1] Univ New S Wales, Dept Gastroenterol, Sydney Childrens Hosp, Sydney, NSW 2031, Australia
[2] Univ New S Wales, Sch Biotechnol & Biomol Sci, Sydney, NSW, Australia
[3] Univ New S Wales, Sch Womens & Childrens Hlth, Sydney, NSW, Australia
关键词
CXC chemokines; gastric epithelial cells; Helicobacter pylori; in vitro;
D O I
10.1111/j.1440-1746.2004.03413.x
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background and Aim: Helicobacter pylori infection of the stomach is commonly associated with infiltration of neutrophils. Gastric epithelial cells are recognized as central mediators of tissue responses to this organism. The aim of the present study was to ascertain patterns of production of three neutrophil chemoattractant chemokines following infection of gastric epithelial cells with H. pylori in vitro. Methods: Two gastric cancer-derived epithelial cell lines were infected with H. pylori organisms of previously defined cagE and cagA status for periods of up to 24 h. The production of three chemokines (interleukin [IL]-8, epithelial neutrophil activating protein [ENA]-78 and growth-related oncogene [GRO]-alpha) over this time was measured in culture supernatants using immunoassays. Results: Both IL-8 and GRO-alpha were produced by both AGS and KATO-III cells in response to H. pylori infection, and in a cag PAI-dependent manner. ENA-78, however, was not increased following H. pylori infection. Conclusions: GRO-alpha is expressed by epithelial cells following H. pylori infection along with IL-8. Both may contribute to neutrophilic infiltration present in gastric mucosa associated with H. pylori infection. In contrast, H. pylori infection does not lead to an increased synthesis of ENA-78, suggesting that this may not be as important in vivo. (C) 2004 Blackwell Publishing Asia Pty Ltd.
引用
收藏
页码:982 / 987
页数:6
相关论文
共 28 条
[1]   Mechanisms involved in Helicobacter pylori-induced interleukin-8 production by a gastric cancer cell line, MKN45 [J].
Aihara, M ;
Tsuchimoto, D ;
Takizawa, H ;
Azuma, A ;
Wakebe, H ;
Ohmoto, Y ;
Imagawa, K ;
Kikuchi, M ;
Mukaida, N ;
Matsushima, K .
INFECTION AND IMMUNITY, 1997, 65 (08) :3218-3224
[2]   Chemokines as novel therapeutic targets in inflammatory diseases [J].
Ajuebor, MN ;
Swain, MG ;
Perretti, M .
BIOCHEMICAL PHARMACOLOGY, 2002, 63 (07) :1191-1196
[3]  
BLASER MJ, 1995, CANCER RES, V55, P562
[4]   cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors [J].
Censini, S ;
Lange, C ;
Xiang, ZY ;
Crabtree, JE ;
Ghiara, P ;
Borodovsky, M ;
Rappuoli, R ;
Covacci, A .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (25) :14648-14653
[5]   INDUCTION OF INTERLEUKIN-8 SECRETION FROM GASTRIC EPITHELIAL-CELLS BY A CAGA NEGATIVE ISOGENIC MUTANT OF HELICOBACTER-PYLORI [J].
CRABTREE, JE ;
XIANG, Z ;
LINDLEY, IJD ;
TOMPKINS, DS ;
RAPPUOLI, R ;
COVACCI, A .
JOURNAL OF CLINICAL PATHOLOGY, 1995, 48 (10) :967-969
[6]  
Crabtree JE, 1998, DIGEST DIS SCI, V43, p46S
[7]   INTERLEUKIN-8 EXPRESSION IN HELICOBACTER-PYLORI INFECTED, NORMAL, AND NEOPLASTIC GASTRODUODENAL MUCOSA [J].
CRABTREE, JE ;
WYATT, JI ;
TREJDOSIEWICZ, LK ;
PEICHL, P ;
NICHOLS, PH ;
RAMSAY, N ;
PRIMROSE, JN ;
LINDLEY, IJD .
JOURNAL OF CLINICAL PATHOLOGY, 1994, 47 (01) :61-66
[8]  
CRABTREE JE, 1994, GUT, V35, P1567
[9]   EXPRESSION OF INTERLEUKIN-8 AND CD54 BY HUMAN GASTRIC EPITHELIUM AFTER HELICOBACTER-PYLORI INFECTION IN-VITRO [J].
CROWE, SE ;
ALVAREZ, L ;
DYTOC, M ;
HUNT, RH ;
MULLER, M ;
SHERMAN, P ;
PATEL, J ;
JIN, Y ;
ERNST, PB .
GASTROENTEROLOGY, 1995, 108 (01) :65-74
[10]   cagE is a virulence factor associated with Helicobacter pylori-induced duodenal ulceration in children [J].
Day, AS ;
Jones, NL ;
Lynett, JT ;
Jennings, HA ;
Fallone, CA ;
Beech, R ;
Sherman, PM .
JOURNAL OF INFECTIOUS DISEASES, 2000, 181 (04) :1370-1375