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 pylori correlated to clinico-histological outcomes and gastric α5β1 integrin expressions. One hundred forty five patients with H. pylori infection and 47 noninfected controls were enrolled to check gastric integrin α5β1 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%CI: 1.8-11.9). H. pylori-infected patients had higher integrin α5β1 than noninfected patients (P < 0.05). Furthermore, cagL-Y58E59 H. pylori infection predisposed an upward shift in integrin α5β1 (P = 0.007) in the corpus, leading to more severe corpus chronic inflammation (P < 0.05). H. pylori CagL amino acid polymorphisms like Y58E59 correlate with a higher risk of GCA, and may regulate a corpus shift of gastric integrin α5β1 to lead to severe corpus gastritis during gastric carcinogenesis.