Helicobacter pylori regulates ILK to influence autophagy through Rac1 and RhoA signaling pathways in gastric epithelial cells

2021 ◽  
pp. 105054
Author(s):  
Zheng Xu ◽  
Boqing Li ◽  
Yunqiu Du ◽  
Ruiqing Zhang ◽  
Xiaohan Tong ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Signaling Pathways ◽  
Gastric Epithelial Cells ◽  
Rhoa Signaling

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 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 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.

Effect of Helicobacter pylori on Cell Gap Junction Ultrastructure of Gastric Epithelial Cells

2009 ◽  
Vol 2009 (6) ◽  
pp. 722-728
Author(s):  
Can-Xia XU ◽  
Yan JIA ◽  
Wen-Bin YANG ◽  
Hui-Fang ZOU ◽  
Fen WANG ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Gap Junction ◽  
Gastric Epithelial Cells

M1959 Helicobacter pylori cagA Tyrosine Phosphorylation Triggers the Interleukin-11/STAT3 Pathway in Gastric Epithelial Cells

2010 ◽  
Vol 138 (5) ◽  
pp. S-448
Author(s):  
Kai Syin Lee ◽  
Anastasia Kalantzis ◽  
Naoko Murata-Kamiya ◽  
Masanori Hatakeyama ◽  
Andrew S. Giraud ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Epithelial Cells ◽  
Tyrosine Phosphorylation ◽  
Gastric Epithelial Cells ◽  
Stat3 Pathway ◽  
Interleukin 11
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