Helicobacter pylori babA2, cagA, and s1 vacA genes work synergistically in causing intestinal metaplasia.
OBJECTIVE
To determine any associations between the Helicobacter pylori genes babA2, oipA, cagA and the s and m alleles of vacA. In addition, to verify whether these genes work synergistically or independently in causing gastritis, peptic ulcer, and intestinal metaplasia.


METHODS
One hundred and sixty seven H pylori positive patients were studied (52 antral gastritis, 41 diffuse gastritis, 41 peptic ulcer, and 33 duodenitis). Helicobacter pylori virulence genes were amplified by means of the polymerase chain reaction.


RESULTS
Significant associations were found between babA2 and the other H pylori genes studied. When considered singly, all the genes were associated with disease diagnosis, inflammation, and intestinal metaplasia. Four H pylori groups were defined. Group A: cagA-, s2m2, babA2-; group B: cagA+, s1m1, babA2+; group C: cagA+, s1m2, babA2+; group D: cagA+, s1m2, babA2-. Group A infecting strains were associated with less severe endoscopic and inflammatory conditions, whereas group B strains were associated with the worst endoscopic and inflammatory findings. Intestinal metaplasia was a rare finding in group A infected patients (< 10%), whereas it was frequent in those infected with group B strains (48%).


CONCLUSIONS
The H pylori genes cagA, oipA "on", s1 and m1 vacA, and babA2 are associated with each other, possibly as a result of shared selective pressure. When coexpressed by the same H pylori strain, cagA, s1 and m1 vacA, and babA2 work synergistically in worsening inflammation. Infections caused by strains coexpressing cagA, s1m1 vacA, and babA2 are those at higher risk for intestinal metaplasia.
Zambon
C-F
CF
Department of Medical and Surgical Sciences, University-Hospital of Padova, Via Giustiniani 2, 35128 Padova, Italy.
Navaglia
F
F
Basso
D
D
Rugge
M
M
Plebani
M
M
D018829:Adhesins, Bacterial; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000942:Antigens, Bacterial / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D002352:Carrier Proteins / Q000235:genetics; D004382:Duodenitis / Q000382:microbiology; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000382:microbiology; D005798:Genes, Bacterial; D016481:Helicobacter Infections / Q000150:complications* / Q000382:microbiology; D016480:Helicobacter pylori / Q000145:classification / Q000235:genetics* / Q000472:pathogenicity; D006801:Humans; D008297:Male; D008679:Metaplasia / Q000382:microbiology; D008875:Middle Aged; D016017:Odds Ratio; D010437:Peptic Ulcer / Q000382:microbiology; D016133:Polymerase Chain Reaction / Q000379:methods; D011230:Precancerous Conditions / Q000382:microbiology*; D013274:Stomach Neoplasms / Q000382:microbiology*; D014774:Virulence / Q000235:genetics
D018829:Adhesins, Bacterial; D000942:Antigens, Bacterial; C400429:BabA protein, Helicobacter pylori; D001426:Bacterial Proteins; D002352:Carrier Proteins; C074689:VacA protein, Helicobacter pylori; C080866:cagA protein, Helicobacter pylori