Matrix metalloproteinase-3 promoter polymorphisms but not dupA-H. pylori correlate to duodenal ulcers in H. pylori-infected females.
BACKGROUND
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.


RESULTS
Of 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.


CONCLUSIONS
The MMP-3 promoter polymorphism, but not the dupA-status, may correlate with susceptibility to duodenal ulcer after H. pylori infection in Taiwanese females.
Yeh
Yi-Chun
YC
Institute of Clinical Medicine, National Cheng Kung University Hospital, Medical College, Tainan, Taiwan.
Cheng
Hsiu-Chi
HC
Chang
Wei-Lun
WL
Yang
Hsiao-Bai
HB
Sheu
Bor-Shyang
BS
D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D044466:Asian People / Q000235:genetics; D004381:Duodenal Ulcer / Q000201:enzymology / Q000235:genetics* / Q000382:microbiology; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D016481:Helicobacter Infections / Q000201:enzymology / Q000235:genetics* / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics* / Q000302:isolation & purification / Q000378:metabolism; D006801:Humans; D008297:Male; D019278:Matrix Metalloproteinase 3 / Q000235:genetics* / Q000378:metabolism; D020782:Matrix Metalloproteinases / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012737:Sex Factors; D013624:Taiwan; D037521:Virulence Factors / Q000235:genetics* / Q000378:metabolism; D055815:Young Adult
C528428:DupA protein, Helicobacter pylori; D037521:Virulence Factors; D020782:Matrix Metalloproteinases; D019278:Matrix Metalloproteinase 3