The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis

Yutaka Minohara, David K. Boyd, Hal K. Hawkins, Peter B. Ernst, Janak Patel, Sheila E. Crowe

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Background: Helicobacter pylori infection leads to gastritis, peptic ulcer, and gastric cancer, in part due to epithelial damage following bacteria binding to the epithelium. Infection with cag pathogenicity island (PAI) bearing strains of H. pylori is associated with increased gastric inflammation and a higher incidence of gastroduodenal diseases. It is now known that various effector molecules are injected into host epithelial cells via a type IV secretion apparatus, resulting in cytoskeletal changes and chemokine secretion. Whether binding of bacteria and subsequent apoptosis of gastric epithelial cells are altered by cag PAI status was examined in this study. Methods: AGS, Kato III, and N87 human gastric epithelial cell lines were incubated with cag PAI-positive or cag PAI-negative strains of H. pylori in the presence or absence of clarithromycin. Binding was evaluated by flow cytometry and scanning electron microscopy. Apoptosis was assessed by detection of DNA degradation and ELISA detection of exposed histone residues. Results: cag PAI-negative strains bound to gastric epithelial cells to the same extent as cag PAI-positive strains. Both cag PAI-positive and cag PAI-negative strains induced apoptosis. However, cag PAI-positive strains induced higher levels of DNA degradation. Incubation with clarithromycin inactivated H. pylori but did not affect binding. However, pretreatment with clarithromycin decreased infection-induced apoptosis. Conclusions: cag PAI status did not affect binding of bacteria to gastric epithelial cells but cag PAI-positive H. pylori induced apoptosis more rapidly than cag PAI-negative mutant strains, suggesting that H. pylori binding and subsequent apoptosis are differentially regulated with regard to bacterial properties.

Original languageEnglish (US)
Pages (from-to)583-590
Number of pages8
JournalHelicobacter
Volume12
Issue number6
DOIs
StatePublished - Dec 2007

Fingerprint

Genomic Islands
Helicobacter pylori
Stomach
Epithelial Cells
Apoptosis
Clarithromycin
Bacteria
DNA
Helicobacter Infections
Gastritis
Infection
Peptic Ulcer
Chemokines
Electron Scanning Microscopy
Histones
Stomach Neoplasms
Flow Cytometry

Keywords

  • Apoptosis
  • Bacterial binding
  • cag PAI
  • Gastric epithelial cells

ASJC Scopus subject areas

  • Gastroenterology
  • Microbiology

Cite this

The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis. / Minohara, Yutaka; Boyd, David K.; Hawkins, Hal K.; Ernst, Peter B.; Patel, Janak; Crowe, Sheila E.

In: Helicobacter, Vol. 12, No. 6, 12.2007, p. 583-590.

Research output: Contribution to journalArticle

Minohara, Yutaka ; Boyd, David K. ; Hawkins, Hal K. ; Ernst, Peter B. ; Patel, Janak ; Crowe, Sheila E. / The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis. In: Helicobacter. 2007 ; Vol. 12, No. 6. pp. 583-590.
@article{e16667cfd4dd4b858bde60da9fb49857,
title = "The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis",
abstract = "Background: Helicobacter pylori infection leads to gastritis, peptic ulcer, and gastric cancer, in part due to epithelial damage following bacteria binding to the epithelium. Infection with cag pathogenicity island (PAI) bearing strains of H. pylori is associated with increased gastric inflammation and a higher incidence of gastroduodenal diseases. It is now known that various effector molecules are injected into host epithelial cells via a type IV secretion apparatus, resulting in cytoskeletal changes and chemokine secretion. Whether binding of bacteria and subsequent apoptosis of gastric epithelial cells are altered by cag PAI status was examined in this study. Methods: AGS, Kato III, and N87 human gastric epithelial cell lines were incubated with cag PAI-positive or cag PAI-negative strains of H. pylori in the presence or absence of clarithromycin. Binding was evaluated by flow cytometry and scanning electron microscopy. Apoptosis was assessed by detection of DNA degradation and ELISA detection of exposed histone residues. Results: cag PAI-negative strains bound to gastric epithelial cells to the same extent as cag PAI-positive strains. Both cag PAI-positive and cag PAI-negative strains induced apoptosis. However, cag PAI-positive strains induced higher levels of DNA degradation. Incubation with clarithromycin inactivated H. pylori but did not affect binding. However, pretreatment with clarithromycin decreased infection-induced apoptosis. Conclusions: cag PAI status did not affect binding of bacteria to gastric epithelial cells but cag PAI-positive H. pylori induced apoptosis more rapidly than cag PAI-negative mutant strains, suggesting that H. pylori binding and subsequent apoptosis are differentially regulated with regard to bacterial properties.",
keywords = "Apoptosis, Bacterial binding, cag PAI, Gastric epithelial cells",
author = "Yutaka Minohara and Boyd, {David K.} and Hawkins, {Hal K.} and Ernst, {Peter B.} and Janak Patel and Crowe, {Sheila E.}",
year = "2007",
month = "12",
doi = "10.1111/j.1523-5378.2007.00537.x",
language = "English (US)",
volume = "12",
pages = "583--590",
journal = "Helicobacter",
issn = "1083-4389",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - The effect of the cag pathogenicity island on binding of Helicobacter pylori to gastric epithelial cells and the subsequent induction of apoptosis

AU - Minohara, Yutaka

AU - Boyd, David K.

AU - Hawkins, Hal K.

AU - Ernst, Peter B.

AU - Patel, Janak

AU - Crowe, Sheila E.

PY - 2007/12

Y1 - 2007/12

N2 - Background: Helicobacter pylori infection leads to gastritis, peptic ulcer, and gastric cancer, in part due to epithelial damage following bacteria binding to the epithelium. Infection with cag pathogenicity island (PAI) bearing strains of H. pylori is associated with increased gastric inflammation and a higher incidence of gastroduodenal diseases. It is now known that various effector molecules are injected into host epithelial cells via a type IV secretion apparatus, resulting in cytoskeletal changes and chemokine secretion. Whether binding of bacteria and subsequent apoptosis of gastric epithelial cells are altered by cag PAI status was examined in this study. Methods: AGS, Kato III, and N87 human gastric epithelial cell lines were incubated with cag PAI-positive or cag PAI-negative strains of H. pylori in the presence or absence of clarithromycin. Binding was evaluated by flow cytometry and scanning electron microscopy. Apoptosis was assessed by detection of DNA degradation and ELISA detection of exposed histone residues. Results: cag PAI-negative strains bound to gastric epithelial cells to the same extent as cag PAI-positive strains. Both cag PAI-positive and cag PAI-negative strains induced apoptosis. However, cag PAI-positive strains induced higher levels of DNA degradation. Incubation with clarithromycin inactivated H. pylori but did not affect binding. However, pretreatment with clarithromycin decreased infection-induced apoptosis. Conclusions: cag PAI status did not affect binding of bacteria to gastric epithelial cells but cag PAI-positive H. pylori induced apoptosis more rapidly than cag PAI-negative mutant strains, suggesting that H. pylori binding and subsequent apoptosis are differentially regulated with regard to bacterial properties.

AB - Background: Helicobacter pylori infection leads to gastritis, peptic ulcer, and gastric cancer, in part due to epithelial damage following bacteria binding to the epithelium. Infection with cag pathogenicity island (PAI) bearing strains of H. pylori is associated with increased gastric inflammation and a higher incidence of gastroduodenal diseases. It is now known that various effector molecules are injected into host epithelial cells via a type IV secretion apparatus, resulting in cytoskeletal changes and chemokine secretion. Whether binding of bacteria and subsequent apoptosis of gastric epithelial cells are altered by cag PAI status was examined in this study. Methods: AGS, Kato III, and N87 human gastric epithelial cell lines were incubated with cag PAI-positive or cag PAI-negative strains of H. pylori in the presence or absence of clarithromycin. Binding was evaluated by flow cytometry and scanning electron microscopy. Apoptosis was assessed by detection of DNA degradation and ELISA detection of exposed histone residues. Results: cag PAI-negative strains bound to gastric epithelial cells to the same extent as cag PAI-positive strains. Both cag PAI-positive and cag PAI-negative strains induced apoptosis. However, cag PAI-positive strains induced higher levels of DNA degradation. Incubation with clarithromycin inactivated H. pylori but did not affect binding. However, pretreatment with clarithromycin decreased infection-induced apoptosis. Conclusions: cag PAI status did not affect binding of bacteria to gastric epithelial cells but cag PAI-positive H. pylori induced apoptosis more rapidly than cag PAI-negative mutant strains, suggesting that H. pylori binding and subsequent apoptosis are differentially regulated with regard to bacterial properties.

KW - Apoptosis

KW - Bacterial binding

KW - cag PAI

KW - Gastric epithelial cells

UR - http://www.scopus.com/inward/record.url?scp=36249004364&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=36249004364&partnerID=8YFLogxK

U2 - 10.1111/j.1523-5378.2007.00537.x

DO - 10.1111/j.1523-5378.2007.00537.x

M3 - Article

C2 - 18001397

AN - SCOPUS:36249004364

VL - 12

SP - 583

EP - 590

JO - Helicobacter

JF - Helicobacter

SN - 1083-4389

IS - 6

ER -