Abstract
BackgroundThis study investigated if the H. pylori dupA genotype and certain host single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), including MMP-3, MMP-7, MMP-9, TIMP-1 and TIMP-2, might correlate with ulcer risk of H. pylori-infected Taiwanese patients.ResultsOf the 549 H. pylori-infected patients enrolled, 470 patients (265 with gastritis, 118 with duodenal ulcer, and 87 with gastric ulcer) received SNPs analysis of MMP-3-1612 6A > 5A, MMP-7-181 A > G, MMP-9exon 6 A > G, TIMP-1372 T > C and TIMP-2-418 G > C by PCR-RFLP. The 181 collected H. pylori isolates were detected for the dupA genotype by PCR. The rates of dupA-positive H. pylori infection were similar among patients with duodenal ulcer (22.8%), gastric ulcer (20.0%), and gastritis (25.5%) (p > 0.05). Males had higher rates of duodenal ulcer and gastric ulcer than females (p < 0.01). Of H. pylori-infected patients, the MMP-3 6A6A genotype were more common in patients with duodenal ulcers than in those with gastritis (87.7% vs. 74.9%, p < 0.05) in females. This genotype had a 2.4-fold (95% CI: 1.02-5.66) increased risk of duodenal ulcer, compared to those with the 5A carrier. Combining the MMP-3/TIMP-1 genotype as 6A6A/CC, the risk of duodenal ulcer increased up to 3.6 fold (p < 0.05) in H. pylori-infected females.ConclusionsThe MMP-3 promoter polymorphism, but not the dupA-status, may correlate with susceptibility to duodenal ulcer after H. pylori infection in Taiwanese females.
Highlights
This study investigated if the H. pylori duodenal ulcer-promoting gene A (dupA) genotype and certain host single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), including MMP-3, MMP-7, MMP-9, TIMP-1 and TIMP-2, might correlate with ulcer risk of H. pylori-infected Taiwanese patients
Two isolates were dupA-positive by single primer pairs
The prevalence rates of dupA-positive H. pylori infection were similar between patients with and those without ulcers (p > 0.05)
Summary
This study investigated if the H. pylori dupA genotype and certain host single nucleotide polymorphisms (SNPs) of matrix metalloproteinases (MMPs) and their inhibitors (TIMPs), including MMP-3, MMP-7, MMP-9, TIMP-1 and TIMP-2, might correlate with ulcer risk of H. pylori-infected Taiwanese patients. Helicobacter pylori infection leads to chronic gastritis and in some individuals, to peptic ulcer disease or even gastric carcinoma [1]. In Taiwan, despite the nearly 100% prevalence of the so-called triple-genopositive cagA-vacA-babA2 virulent H. pylori infections, there is a lack of correlation to different disease outcomes [4,5]. It will be useful for Taiwan to validate new virulence factors or any host genomic predisposition in relation to severe H. pylori-infected clinical outcomes. H. pylori infection stimulates the production of proinflammatory cytokines, such as IL-1, which play important roles in gastric inflammation and physiology. IL-1 beta or IL-1RN polymorphisms are not associated with gastric ulcer in the Taiwanese population [12]
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