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Infection and Immunity, January 2001, p. 81-88, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.81-88.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Comparison of CXC Chemokines ENA-78 and Interleukin-8 Expression in Helicobacter pylori-Associated Gastritis

Gabriele Rieder,1,2 Wolfgang Einsiedl,1 Rudolf A. Hatz,2 Manfred Stolte,3 Georg A. Enders,1 and Alfred Walz4,*

Institute for Surgical Research1 and Department of Surgery,2 Klinikum Grosshadern, Ludwig-Maximilians University, Munich, and Department of Pathology, Klinikum Bayreuth, Bayreuth,3 Germany, and Theodor Kocher Institute, University of Bern, Bern, Switzerland4

Received 28 March 2000/Returned for modification 4 May 2000/Accepted 3 October 2000

Colonization of the gastric mucosa with Helicobacter pylori is associated with a dense infiltration of granulocytes into the lamina propria in the active phase of gastritis. In this study, we investigated the involvement of epithelial cell-derived neutrophil-activating protein 78 (ENA-78) in development of H. pylori-associated gastritis. Antral biopsies from 27 patients with H. pylori-associated gastritis and 25 from H. pylori-negative individuals were first analyzed for ENA-78 and interleukin-8 (IL-8) mRNA by semiquantitative reverse transcription (RT)-PCR. In H. pylori-positive patients, significantly elevated levels were found for both chemokines (P < 0.05). Only IL-8 mRNA levels differed significantly (P < 0.05) in H. pylori-infected individuals who had serum antibodies for cytotoxin-associated protein CagA versus H. pylori-infected CagA-negative persons. Quantification of ENA-78 transcript levels by competitive RT-PCR yielded a significant 45-fold upregulation for ENA-78 transcripts in biopsies of H. pylori-positive versus H. pylori-negative patients (P < 0.05). In contrast to earlier findings with IL-8, the degree of ENA-78 mRNA upregulation was independent of the grade of activity of gastritis. Immunofluorescence studies on tissues of antral biopsies localized ENA-78 protein expression mainly to the gastric epithelium of H. pylori-positive patients, while control tissues were negative. Upregulation of ENA-78 and IL-8 mRNA and protein expression was also observed in an in vitro system using a gastric adenocarcinoma cell line. Only viable H. pylori yielded a strong ENA-78 and IL-8 induction, while H. pylori outer membrane proteins or water-soluble proteins had no significant effect. These data provide evidence for the importance of both IL-8 and ENA-78 in the development and perpetuation of H. pylori-associated gastritis.

* Corresponding author. Mailing address: Theodor Kocher Institute, University of Bern, Freiestrasse 1, CH-3012 Bern, Switzerland. Phone: (41) 31 631-4166. Fax: (41) 31 631-4145. E-mail: alfred.walz{at}tki.unibe.ch.

Infection and Immunity, January 2001, p. 81-88, Vol. 69, No. 1
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.1.81-88.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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