CagA+ Helicobacter pylori induces greater levels of prostaglandin E 2 than cagA− strains

Abstract

cagA+ Helicobacter pylori (HP) infection is associated with an increased risk of distal gastric cancer. Previous studies investigating the effect of HP infection on prostaglandin E 2 (PGE 2) levels have not differentiated between cagA+ and cagA− strains and consequently have produced contradictory results. The aim was to investigate the effect of cagA+ strains on PGE 2 and enhance the understanding of the mechanisms leading to gastric diseases. Hundred patients without peptic ulcers and not on medication were recruited (one later excluded) from endoscopy clinics: six biopsies were obtained from each patient. PGE 2, colonization density and histology were determined. In addition, HP status was assessed by histology, CLOtest and culture with cagA+ being determined by PCR. Sixty-nine patients were HP− and 30 HP+ (10 cagA+, 18 cagA−, 2 undetermined). In age and sex-matched patients, PGE 2 was significantly greater ( P=0.04) in HP+ (37.2±1.2 pg/mg per 20 min) than in HP− (22.6±1.2). In patients without atrophy, those infected with cagA+ had significantly higher ( P=0.03) PGE 2 levels (53±1.1) than HP−patients (22.6±1.1) and greater levels ( P=0.29) than cagA− patients (35±1.3). In conclusion, the increased levels of PGE 2 in the presence of cagA+ infection could be an important factor by which cagA+ strains enhance the gastric mucus layer protective functions leading to established colonization, gastritis and increased risk of gastric cancer. However, further evaluation with a large-scale multi-centre study is required to substantiate this hypothesis.