Mutation of iceA in Helicobacter pylori compromised IL-8 induction from human gastric epithelial cells.
J Basic Microbiol
; 50 Suppl 1: S83-8, 2010 Dec.
Article
em En
| MEDLINE
| ID: mdl-20806247
ABSTRACT
IceA of Helicobacter pylori (H. pylori) has been suggested as a virulence factor for the bacteria, but its pathogenic role remains unelucidated. Here, we examined the effect of iceA mutation on the secretion of IL-8 by human gastric epithelial cells. We also investigated whether the changes in IL-8 production caused by iceA mutation were associated with impaired adherence of H. pylori to the epithelial cells or with impaired apoptosis of these cells. The iceA mutant strain was constructed from wildtype H. pylori strain by insertional mutagenesis of iceA. The human gastric epithelial cells SGC7901 were infected with wildtype or mutant H. pylori for appropriate lengths of time. The adherence of the bacteria to the epithelial cells was examined by fluorescent microscopy using an anti-H. pylori antibody and flow cytometry. The apoptosis of the epithelial cells was studied by annexin-V staining and flow cytometry. The production of IL-8 by SGC 7901 cells was determined by ELISA. We found that iceA mutation was associated with significantly impaired production of IL-8 from the epithelial cells, which was not due to impaired adherence by the bacteria to the epithelial cells as wildtype and mutant H. pylori exhibited similar levels of binding to the epithelial cells. Furthermore, inactivation of iceA did not affect the apoptotic cell death of SGC7901. Our findings indicate that iceA may contribute to the pathogenicity of H. pylori by modulating the production of IL-8 by host epithelial cells.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Proteínas da Membrana Bacteriana Externa
/
Interleucina-8
/
Helicobacter pylori
/
Infecções por Helicobacter
/
Células Epiteliais
/
Mucosa Gástrica
Limite:
Humans
Idioma:
En
Revista:
J Basic Microbiol
Assunto da revista:
MICROBIOLOGIA
Ano de publicação:
2010
Tipo de documento:
Article
País de afiliação:
China