scholarly journals Helicobacter pylori Induces AGS Cell Motility and Elongation via Independent Signaling Pathways

2004 ◽  
Vol 72 (6) ◽  
pp. 3646-3649 ◽  
Author(s):  
Stefan Moese ◽  
Matthias Selbach ◽  
Terry Kwok ◽  
Volker Brinkmann ◽  
Wolfgang König ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Cell Motility ◽  
Signaling Pathways ◽  
Pathogenicity Island ◽  
Gastric Epithelial Cells ◽  
Cytoskeletal Responses

ABSTRACT Helicobacter pylori induces motogenic and cytoskeletal responses in gastric epithelial cells. We demonstrate that these responses can be induced via independent signaling pathways that often occur in parallel. The cag pathogenicity island appears to be nonessential for induction of motility, whereas the elongation phenotype depends on translocation and phosphorylation of CagA.

scholarly journals Inflammatory signaling pathways induced by Helicobacter pylori in primary human gastric epithelial cells

2016 ◽  
Vol 23 (2) ◽  
pp. 165-174 ◽  
Author(s):  
Cong Tri Tran ◽  
Magali Garcia ◽  
Martine Garnier ◽  
Christophe Burucoa ◽  
Charles Bodet
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Signaling Pathways ◽  
Post Infection ◽  
Gastric Epithelial Cells ◽  
Inflammatory Signaling ◽  
Independent Manner ◽  
Chemokine Production ◽  
H Pylori

Inflammatory signaling pathways induced by Helicobacter pylori remain unclear, having been studied mostly on cell-line models derived from gastric adenocarcinoma with potentially altered signaling pathways and nonfunctional receptors. Here, H. pylori-induced signaling pathways were investigated in primary human gastric epithelial cells. Inflammatory response was analyzed on chemokine mRNA expression and production after infection of gastric epithelial cells by H. pylori strains, B128 and B128Δ cagM, a cag type IV secretion system defective strain. Signaling pathway involvement was investigated using inhibitors of epidermal growth factor receptor (EGFR), MAPK, JAK and blocking Abs against TLR2 and TLR4. Inhibitors of EGFR, MAPK and JAK significantly reduced the chemokine mRNA expression and production induced by both H. pylori strains at 3 h and 24 h post-infection. JNK inhibitor reduced chemokine production at 24 h post-infection. Blocking Abs against TLR2 but not TLR4 showed significant reduction of chemokine secretion. Using primary culture of human gastric epithelial cells, our data suggest that H. pylori can be recognized by TLR2, leading to chemokine induction, and that EGFR, MAPK and the JAK/STAT signaling pathways play a key role in the H. pylori-induced CXCL1, CXCL5 and CXCL8 response in a cag pathogenicity island-independent manner.

scholarly journals Helicobacter pylori regulates ILK signaling pathways to influence autophagy in gastric epithelial cells

2020 ◽  
Author(s):  
Zheng Xu ◽  
Yunqiu Du ◽  
Ruiqing Zhang ◽  
Xiaohan Tong ◽  
Boqing Li ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Negative Correlation ◽  
Signal Molecules ◽  
Gastric Epithelial Cells ◽  
Marker Protein ◽  
Autophagosome Formation ◽  
H Pylori ◽  
Rhoa Signaling

Abstract BackgroundThe ability of Helicobacter pylori to manipulate host autophagy is an important pathogenic mechanism.ResultsWe found a negative correlation between the expression of ILK and the autophagy marker protein LC3B in H. pylori-positive human samples and in H. pylori-infected GES-1 cell lines. There was a significant accumulation of autophagosomes in ILK-knockdown GES-1 cells, and the expression levels of both LC3B and p62 were also increased. Here, we showed the activities of Rac1 and RhoA were decreased in H. pylori-infected GES-1 cells and ILK-knockdown GES-1 cells. Inhibition of Rac1 and RhoA increased LC3B levels and autophagosome formation in GES-1 cells after H. pylori infection. Simultaneously, H. pylori infection activated downstream signal molecules of Rac1 (PAK1, LIMK1 and cofilin) and RhoA (ROCK1, ROCK2 and LIMK1 and cofilin).ConclusionsOur results demonstrated that H. pylori regulated autophagy through ILK/Rac1 and ILK/RhoA signaling pathways in gastric epithelial cells.

scholarly journals Proteins Encoded by the cagPathogenicity Island of Helicobacter pylori Are Required for NF-κB Activation

1998 ◽  
Vol 66 (5) ◽  
pp. 2346-2348 ◽  
Author(s):  
Erik Glocker ◽  
Christina Lange ◽  
Antonello Covacci ◽  
Stefan Bereswill ◽  
Manfred Kist ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Transcription Factor ◽  
Epithelial Cells ◽  
Gene Cluster ◽  
Pathogenicity Island ◽  
Gastric Epithelial Cells ◽  
Bacterial Gene ◽  
Cluster A ◽  
The Difference ◽  
H Pylori

ABSTRACT Helicobacter pylori is the etiological agent in the development of chronic gastritis, duodenal ulceration, and gastric adenocarcinoma. The difference in virulence between individual strains is reflected in their ability to induce interleukin-8 (IL-8) secretion from gastric epithelial cells. It has been shown that virulence is associated with the presence of a bacterial gene cluster (a pathogenicity island). We have recently demonstrated that H. pylori-mediated IL-8 secretion requires activation of the transcription factor NF-κB. Here, we show that NF-κB induction requires six membrane proteins encoded within the pathogenicity island.

scholarly journals cDNA Array Analysis of cag Pathogenicity Island-Associated Helicobacter pylori Epithelial Cell Response Genes

2001 ◽  
Vol 69 (11) ◽  
pp. 6970-6980 ◽  
Author(s):  
Joanne M. Cox ◽  
Christopher L. Clayton ◽  
Toshihiko Tomita ◽  
Don M. Wallace ◽  
Philip A. Robinson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Cdna Array ◽  
Pathogenicity Island ◽  
High Density ◽  
Differentially Expressed ◽  
Gastric Epithelial Cells ◽  
H Pylori

ABSTRACT Helicobacter pylori strains containing thecag pathogenicity island (PAI) induce NF-κB activation and interleukin-8 secretion in gastric epithelial cells. The aim of this study was to investigate changes in epithelial gene expression induced by cag PAI-positive and -negative strains ofH. pylori using high-density cDNA array hybridization technology. Radio-labeled cDNA prepared from H. pylori-infected Kato 3 gastric epithelial cells was hybridized to high-density cDNA arrays to identify changes in epithelial gene expression compared to noninfected controls. In vivo expression of selected, differentially expressed genes was examined by reverse transcription-PCR analysis of H. pylori-positive and -negative gastric mucosa. Screening of ca. 57,800 cDNAs identified 208 known genes and 48 novel genes and/or expressed sequence tags of unknown function to be differentially expressed in Kato 3 cells following H. pylori infection. Marked differences in gene expression profiles were observed following cagPAI-positive and cag PAI-negative infection with 15 novel cDNAs and 92 known genes being differentially expressed. H. pylori was found to change the expression of genes encoding growth factors and cytokine/chemokines and their receptors, apoptosis proteins, transcription factors and metalloprotease-disintegrin proteins (ADAMs), and tissue inhibitors of metalloproteinases. Gastric differential expression of selected known genes (amphiregulin and ADAM 10) and a novel gene (HPYR1) was confirmed in vivo in patients with H. pylori infection. Confirmation of the in vivo expression of selected genes demonstrates the usefulness of this approach for investigating pathogen-induced changes in host gene expression.

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