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Infection and Immunity, August 2001, p. 5001-5009, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.5001-5009.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Epithelial Intestinal Cell Apoptosis Induced by Helicobacter pylori Depends on Expression of the cag Pathogenicity Island Phenotype

Gaëlle Le'Negrate,1 Vittorio Ricci,2,3 Véronique Hofman,4 Baharia Mograbi,1 Paul Hofman,1,4 and Bernard Rossi1,*

INSERM 3641 and INSERM 452,2 IFR 50, and Department of Pathology, Faculty of Medicine,4 06107 Nice Cedex 01, France, and Institute of Human Physiology, University of Pavia Medical School, 27100 Pavia, Italy3

Received 15 February 2001/Returned for modification 10 April 2001/Accepted 10 May 2001

Helicobacter pylori has been shown to induce chronic active gastritis and peptic ulcer and may contribute to the development of duodenal ulcer. Previous studies have shown that H. pylori mediates apoptosis of gastric epithelial cells via a Fas-dependent pathway. However, evidence for the induction of such a mechanism in intestinal epithelial cells (IEC) by H. pylori infection has not been demonstrated yet. This study was performed (i) to ascertain that H. pylori can induce IEC apoptosis; (ii) to delineate the role of the cag pathogenicity island (PAI), cagE, and vacA gene products in this process; and (iii) to verify whether the Fas-dependent pathway is involved in this phenomenon. When T84 cells were exposed to VacA+/cag PAI+ H. pylori strains (CCUG 17874 and 60190), they exhibited apoptosis hallmarks as assessed by morphological studies, as well as annexin V and 3,3'-dihexyloxacarbocyanine iodide staining. In contrast, few or no apoptotic features could be detected after incubation with an isogenic mutant of strain 60190 in which the cagE gene was disrupted (60190:C- strain) or with a VacA-/cag PAI- H. pylori strain (G21). In addition, activation of caspase-3 during infection with VacA+/cag PAI+ H. pylori strains was inhibited by pretreatment of IEC with an antagonistic anti-Fas antibody (ZB4). Taken together, these findings indicate that H. pylori triggers apoptosis in IEC via a Fas-dependent pathway following a process that depends on the expression of the cag PAI.

* Corresponding author. Mailing address: INSERM 364, Faculté de Médecine, Ave. de Valombrose, 06107 Nice Cedex 01, France. Phone: 33 4 93 37 77 02/03. Fax: 33 4 93 81 94 56. E-mail: rossi{at}unice.fr.

Infection and Immunity, August 2001, p. 5001-5009, Vol. 69, No. 8
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.8.5001-5009.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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