Toward the Understanding of Molecular Aspects of Helicobacter Pylori cag-PAI

2011 ◽  
pp. 311-334
Keyword(s):  
Helicobacter Pylori ◽  
Molecular Aspects ◽  
Cag Pai

scholarly journals Diagnosis of Helicobacter pylori infection: a look into molecular aspects of urea breath test

2019 ◽  
Vol 31 (3) ◽  
Author(s):  
Chiara Marinoni ◽  
Davide G. Ribaldone ◽  
Chiara Rosso ◽  
Marco Astegiano ◽  
Gian Paolo Caviglia
Keyword(s):  
Helicobacter Pylori ◽  
Breath Test ◽  
Urea Breath Test ◽  
Helicobacter Pylori Infection ◽  
Molecular Aspects

Status of Helicobacter pylori cag pathogenicity island ( cag PAI) integrity and significance of its individual genes

2018 ◽  
Vol 59 ◽  
pp. 167-171 ◽  
Author(s):  
Rumyana Markovska ◽  
Lyudmila Boyanova ◽  
Daniel Yordanov ◽  
Petya Stankova ◽  
Galina Gergova ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Pathogenicity Island ◽  
Cag Pathogenicity Island ◽  
Cag Pai

scholarly journals Helicobacter pylori with East Asian-type cag PAI genes is more virulent than strains with Western-type in some cag PAI genes

2017 ◽  
Vol 48 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Xiao-yan Yuan ◽  
Jin-Jun Yan ◽  
Ya-chao Yang ◽  
Chun-mei Wu ◽  
Yan Hu ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
East Asian ◽  
Cag Pai

Association of Cag PAI integrity with severeness of Helicobacter pylori infection in patients with gastritis

2015 ◽  
Vol 63 (6) ◽  
pp. 252-257 ◽  
Author(s):  
A. Ahmadzadeh ◽  
H. Ghalehnoei ◽  
N. Farzi ◽  
A. Yadegar ◽  
M. Alebouyeh ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Helicobacter Pylori Infection ◽  
Cag Pai

scholarly journals Paxillin is a novel cellular target for converging Helicobacter pylori-induced cellular signaling

2011 ◽  
Vol 301 (4) ◽  
pp. G601-G611 ◽  
Author(s):  
Fazal H. Tabassam ◽  
David Y. Graham ◽  
Yoshio Yamaoka
Keyword(s):  
Helicobacter Pylori ◽  
Kinase Activity ◽  
Stress Fiber ◽  
Fiber Formation ◽  
Actin Stress Fiber ◽  
Stress Fiber Formation ◽  
Cellular Target ◽  
H Pylori ◽  
Actin Stress Fiber Formation ◽  
Cag Pai

Paxillin is involved in the regulation of Helicobacter pylori -mediated gastric epithelial cell motility. We investigated the signaling pathways regulating H. pylori -induced paxillin phosphorylation and the effect of the H. pylori virulence factors cag pathogenicity island (PAI) and outer inflammatory protein (OipA) on actin stress fiber formation, cell phenotype, and IL-8 production. Gastric cell infection with live H. pylori induced site-specific phosphorylation of paxillin tyrosine (Y) 31 and Y118 in a time- and concentration-dependent manner. Activated paxillin localized in the cytoplasm at the tips of H. pylori -induced actin stress fibers. Isogenic oipA mutants significantly reduced paxillin phosphorylation at Y31 and Y118 and reduced actin stress fiber formation. In contrast, cag PAI mutants only inhibited paxillin Y118 phosphorylation. Silencing of epidermal growth factor receptor (EGFR), focal adhesion kinase (FAK), or protein kinase B (Akt) expression by small-interfering RNAs or inhibiting kinase activity of EGFR, Src, or phosphatidylinositol 3-kinase (PI3K) markedly reduced H. pylori -induced paxillin phosphorylation and morphologic alterations. Reduced FAK expression or lack of Src kinase activity suppressed H. pylori -induced IL-8 production. Compared with infection with the wild type, infection with the cag PAI mutant and oipA mutant reduced IL-8 production by nearly 80 and 50%. OipA-induced IL-8 production was FAK- and Src-dependent, although a FAK/Src-independent pathway for IL-8 production also exists, and the cag PAI may be mainly involved in this pathway. We propose paxillin as a novel cellular target for converging H. pylori -induced EGFR, FAK/Src, and PI3K/Akt signaling to regulate cytoskeletal reorganization and IL-8 production in part, thus contributing to the H. pylori -induced diseases.

scholarly journals Prevalence and Diversity of Cag (PAI) in Helicobacter pylori: Study on Gastric Ulcer

2018 ◽  
Vol 08 (03) ◽  
Author(s):  
Firouzeh Morshedzadeh ◽  
Hossein Abbasinia ◽  
Davood Zaeifi
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Ulcer ◽  
Cag Pai

The infection with Helicobacter pylori cag-PAI+ strains modulates in vivo interleukin-4 mRNA expression in human gastric mucosa

2001 ◽  
Vol 120 (5) ◽  
pp. A707-A707
Author(s):  
B ORSINI ◽  
B OTTANELLI ◽  
S CENSINI ◽  
C VACCINES ◽  
G PELLEGRINI ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Mrna Expression ◽  
Interleukin 4 ◽  
Human Gastric Mucosa ◽  
Cag Pai

Human Gastric Epithelium Produces IL-4 and IL-4δ2 Isoform Only upon Helicobacter Pylori Infection

2007 ◽  
Vol 20 (4) ◽  
pp. 809-818 ◽  
Author(s):  
B. Orsini ◽  
J.R. Vivas ◽  
B. Ottanelli ◽  
A. Amedei ◽  
E. Surrenti ◽  
...  
Keyword(s):  
Immune Response ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Healthy Subjects ◽  
Fine Tuning ◽  
Gastric Epithelium ◽  
Gastric Epithelial Cells ◽  
H Pylori ◽  
Cag Pai

Recent evidence suggests that interleukin-4 (IL-4) is related to mucosal tolerance by which an injurious immune response is prevented, suppressed or shifted to a non-injurious response. We investigated the expression of IL-4 and its splice variant isoform IL-4δ2 in gastric epithelial cells of healthy subjects and gastritis patients infected with Helicobacter pylori (H. pylori) with or without the cag pathogenicity island ( cag-PAI). IL-4 and IL-4δ2 mRNAs were evaluated in microdissected gastric epithelium and in AGS cell lines co-cultured with H. pylori B128 or SSI strains. IL-4 mRNA was consistently detected in microdissected gastric epithelial cells from healthy subjects. The IL-4 mRNA expression was low in H. pylori-infected patients, and markedly reduced in cag-PAI-positive ones. IL-4δ2 mRNA was expressed on gastric epithelium of H. pylori-infected patients, but not in healthy subjects. The IL-452 expression was lower in cag-PAI-positive than in cag-PAI-negative H. pylori infected patients. AGS cells also produced IL-4 mRNA upon SSI strain stimulation, whereas IL-4δ2 mRNA expression was detected in AGS co-cultured with either SSI or B128 strains. An inverse correlation was documented between IL-4 and IL-482 mRNA expression by microdissected gastric epithelial cells and the score of gastritis. IL-4, but not IL-452, is expressed by gastric epithelium of healthy subjects, whereas IL-452 and lesser IL-4 mRNA are detectable in the gastric epithelium of H. pylori-infected patients. Data suggest that gastric epithelial cells might regulate the balance between tolerance and immune response by the fine tuning of IL-4 and IL-4δ2 expression.

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