scholarly journals Nucleotide Binding Oligomerization Domain 1 Is an Essential Signal Transducer in Human Epithelial Cells Infected with Helicobacter pylori That Induces the Transepithelial Migration of Neutrophils

Gut and Liver ◽  
2015 ◽  
Vol 9 (3) ◽  
Author(s):  
Beom Jin Kim ◽  
Jae Yeol Kim ◽  
Eung Soo Hwang ◽  
Jae Gyu Kim
2005 ◽  
Vol 11 (3) ◽  
pp. 129-135
Author(s):  
Atsushi Toyoda ◽  
Makoto Hasegawa ◽  
Atsushi Toyoda ◽  
Takako Osaki ◽  
Tomoko Hanawa ◽  
...  

2010 ◽  
Vol 138 (5) ◽  
pp. S-270
Author(s):  
Jae G. Kim ◽  
Beom Jin Kim ◽  
Ki Sung Kim ◽  
Hyoung-Chul Oh ◽  
Jeong Wook Kim

2011 ◽  
Vol 3 (1) ◽  
pp. 35
Author(s):  
Zheng-Xiang Wang ◽  
Hou-Feng Shen ◽  
Hong-Ju Chen

2018 ◽  
Author(s):  
Lennart Pfannkuch ◽  
Robert Hurwitz ◽  
Jan Traulsen ◽  
Paul Kosma ◽  
Monika Schmid ◽  
...  

AbstractThe gastric pathogen Helicobacter pylori activates the NF-κB pathway in human epithelial cells via the α-kinase 1 (Alpk1)–TIFA axis. We and others have previously shown that heptose 1,7-bisphosphate (HBP) acts as a pathogen-associated molecular pattern (PAMP). HBP is an intermediate of lipopolysaccharide (LPS) synthesis in H. pylori and other gram-negative bacteria. Deletion of the hldE (rfaE) gene encoding the enzyme responsible for HBP synthesis, as well as deletion of further upstream genes, causes loss of NF-κB stimulation by H. pylori, while deletion of the downstream phosphatase encoding gene gmhB does not. This has led to the conclusion that HBP is the PAMP responsible for NF-κB induction. Here, our attempts to identify HBP in lysates of H. pylori revealed surprisingly low amounts that fail to explain NF-κB activation. Instead, we identified ADP heptose, a major downstream metabolite of HdlE, as the predominant PAMP in H. pylori lysates, exhibiting ∼100-fold stronger activity compared to HBP. It therefore appears that synthesis of ADP heptose from HBP in H. pylori occurs independently of GmhB. The data lead us to conclude that ADP heptose constitutes the key PAMP, secreted via the pathogen’s cagPAI encoded type 4 secretion (T4SS).


2010 ◽  
Vol 93 (10) ◽  
pp. 4526-4534 ◽  
Author(s):  
Y. Shirasawa ◽  
H. Shibahara-Sone ◽  
T. Iino ◽  
F. Ishikawa

2008 ◽  
Vol 134 (4) ◽  
pp. A-568
Author(s):  
Jae G. Kim ◽  
Bum Joon Park ◽  
Su Yeon Rhie ◽  
Ki Sung Kim ◽  
Sill Moo Park

Author(s):  
Shantal Lizbeth Baltierra‐Uribe ◽  
Alejandra Montañez‐Barragán ◽  
Héctor Romero‐Ramírez ◽  
Ksenia Klimov‐Kravtchenko ◽  
Karla Ivette Martínez‐Pedro ◽  
...  

2021 ◽  
Vol 30 (3) ◽  
pp. 9-19
Author(s):  
Enas M. Ghoneim ◽  
Eman H. Hassan ◽  
Hassan Zaghla ◽  
Doha Taie ◽  
Samah M. Awad

Background: Chronic infection with Helicobacter pylori (H.pylori ) causes atrophic and even gastric metaplastic changes, and it has a well-known link to peptic ulceration. Nucleotide-binding oligomerization domain-containing protein 1 (NOD1) is a protein receptor that is presented by the NOD1 gene. It distinguishes H.pylori bacterial molecules and enhances an immune response Objectives: to describe the relation between the NOD1 gene (rs2075820) polymorphism and H.pylori infection in hepatic and non hepatic patients with chronic gastritis, study its impact on the degree of chronic gastritis in H.pylori positive individuals, and to examine the effect of H. pylori on clinical, endoscopic and histopathological findings and child paugh scoring in hepatic patients. Methodology: Gastric tissue samples were taken from selected 200 patients with chronic gastritis, either hepatic or non hepatic. Rapid urease test and pathological findings classified them into H.pylori infected and non infected patients. Genotyping of NOD 1 was studied using polymerase chain reaction /restriction fragment length polymorphism (PCR–RFLP) method. Results: A significant higher frequency of AA genotype, and the A allele of NOD1 gene in H.pylori +ve patients, either hepatic; (58%)-(73%) or non hepatic;(62%)-(78%) as compared to H.pylori –ve patients,(P <0.001). A highly significant relation between NOD1 genotypes and endoscopic findings, where most of H.pylori infected patients with AA genotype had more peptic ulcer, antral erosion, gastric prolapse, esophageal varices and esophageal hiatus hernia compared to patients with GA and GG genotypes, (P<0.001). No significant impact of H.pylori on signs of liver affection and child paugh scoring in hepatic patients. Conclusions: In NOD1 gene polymorphism, AA genotype and A allele have significantly implicated in H.pylori infection susceptibility and progression. While GG genotype and G allele have a protective effect against H.pylori infection.


2006 ◽  
Vol 176 (6) ◽  
pp. 3796-3803 ◽  
Author(s):  
Yoshihiro Hirata ◽  
Tomoya Ohmae ◽  
Wataru Shibata ◽  
Shin Maeda ◽  
Keiji Ogura ◽  
...  

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