H. pylori isolates with amino acid sequence polymorphisms as presence of both HtrA-L171 & CagL-Y58/E59 increase the risk of gastric cancer

Background H. pylori CagL-Y58/E59 increase gastric cancer risk by stronger binding with integrin to faciliate type IV secretory system (T4SS). H. pylori can secrete high temperature requirement A (HtrA) to mediate E-Cadherin cleavage for gastric epithelial junction disruption, so H. pylori CagL can...

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Vydáno v:Journal of biomedical science Ročník 26; číslo 1; s. 4 - 8
Hlavní autoři: Yeh, Yi-Chun, Kuo, Hsin-Yu, Chang, Wei-Lun, Yang, Hsiao-Bai, Lu, Cheng-Chan, Cheng, Hsiu-Chi, Wu, Ming-Shiang, Sheu, Bor-Shyang
Médium: Journal Article
Jazyk:angličtina
Vydáno: London BioMed Central 05.01.2019
BioMed Central Ltd
Springer Nature B.V
BMC
Témata:
Amino acid sequence
Amino acid sequencing
Amino acids
Binding sites
Biomedical and Life Sciences
Biomedicine
CagL
Cancer
Care and treatment
Clinical outcomes
Complications and side effects
Development and progression
Disruption
Dyspepsia
E-cadherin
Endoscopy
Epithelium
Gastric cancer
Gastroenterology
Gene sequencing
Genetic polymorphisms
H. pylori
Health risks
Helicobacter infections
Helicobacter pylori
High temperature
Histology
HtrA
Infections
Kinases
Leucine
Mutation
Peptic ulcers
Polymerase chain reaction
Proteins
Risk
Risk factors
Stomach cancer
Temperature requirements
Type IV secretory system
Ulcers
Upgrading
Taiwan
HtrA
Type IV secretory system
CagL
Gastric cancer
H. pylori
ISSN:1423-0127, 1021-7770, 1423-0127
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Shrnutí:Background H. pylori CagL-Y58/E59 increase gastric cancer risk by stronger binding with integrin to faciliate type IV secretory system (T4SS). H. pylori can secrete high temperature requirement A (HtrA) to mediate E-Cadherin cleavage for gastric epithelial junction disruption, so H. pylori CagL can adhere to integrin located on basolateral side of epithelium. The study test whether H. pylori HtrA amino acid polymorphisms can increase gastric cancer risk synergistically with CagL-Y58/E59. Methods One-hundred and sixty-four H. pylori -positive patients, including 71 with non-ulcer dyspepsia (NUD), 63 with peptic ulcers (PU), and 30 with gastric cancers (GC), were enrolled to receive upper gastrointestinal endoscopy to obtain gastric biopsies for H. pylori culture and histology by the updated Sydney system. Each isolate was screened for htrA & cagL genotype by polymerase chain reaction and HtrA & CagL-Y58/E59 amino acid sequence polymorphisms by sequencing. Results The prevalence rates of htrA & cagL gene were both 100%. The HtrA amino acid sequence polymorphisms were not different between NUD and PU. The H. pylori isolates of GC had higher rates of HtrA residue 171 as leucine than those of NUD (73.3% vs. 50.7%, P  = 0.036, OR[95%CI] = 2.7[1.1–6.8]). The risk of the H. pylori -infected subjects to get gastric cancer was increased up to 15.4-fold, if the infected isolates had presence of both HtrA-L171 and CagL-Y58/E59 ( P  < 0.001). Conclusions The H. pylori isolates of gastric cancer subjects had a higher rate of HtrA-L171. H. pylori isolates with presence of both HtrA-171 & CagL-Y58/E59 can synergistically increase the risk of gastric cancer.
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ISSN:1423-0127
1021-7770
1423-0127
DOI:10.1186/s12929-019-0498-9