H. pylori cagL Amino Acid Sequence Polymorphism Y58E59 Induces a Corpus Shift of Gastric Integrin α5β1 Related With Gastric Carcinogenesis

We tested whether cagL amino acid sequence polymorphisms of Helicobacter pylon correlated to clinico-histological outcomes and gastric alpha 5 beta 1 integrin expressions. One hundred forty five patients with H. pylori infection and 47 noninfected controls were enrolled to check gastric integrin alpha 5 beta 1 intensities topographically. The collected isolates were screened for cagL-genotype by polymerase chain reaction (PCR), and assessed for amino acid sequence polymorphisms using sequence translation. Our H. pylori isolates were predominantly (98.6%) cagL-genopositive, 95.8% of which had the RGD motif in their amino acid sequences. The isolates from the gastric cancer (GCA) patients indicated a higher rate of amino acid sequence polymorphisms-Y58 and E59-than those of the non-GCA patients (P < 0.05). The polymorphisms as Y58E59 noted with increased risk of GCA up to 4.6-fold (95%Cl: 1.8-11.9). H. pylon-infected patients had higher integrin alpha 5 beta 1 than noninfected patients (P < 0.05). Furthermore, cagL-Y58E59 H. pylori infection predisposed an upward shift in integrin alpha 5 beta 1 (P = 0.007) in the corpus, leading to more severe corpus chronic inflammation (P < 0.05). H. pylon CagL amino acid polymorphisms like Y58E59 correlate with a higher risk of GCA, and may regulate a corpus shift of gastric integrin alpha 5 beta 1 to lead to severe corpus gastritis during gastric carcinogenesis. (C) 2011 Wiley-Liss, Inc.