Polymorphonuclear oxidative burst after Helicobacter pylori water extract stimulation is not influenced by the cytotoxic genotype but indicates infection and gastritis grade

H. pylori-associated gastric mucosal inflammation is characterized by the p resence of polymorphonuclear (PMN) leukocyte infiltrate, which is more seve re when the infecting strain is cagA positive. After appropriate stimuli, s uch as bacterial products, PMN release large amounts of oxygen derived free radicals and proteases, to kill the bacterium. H. pylori seems to be parti cularly resistant to the oxidative machinery of PMN, which can in turn dama ge the host gastric mucosa. We evaluated peripheral PMN oxidative burst res ponse after stimulation with water extracts from cagA positive (WEcagA+) or negative (WEcagA-) H. pylori strains in infected (n=31) and non-infected p atients (n=32) in comparison with healthy controls (n=16); the influence of gastric mucosal inflammatory infiltrate and activity grade on PMN oxidativ e burst were also assessed. PMN oxidative burst was measured by FAGS analys is. H. pylori water extracts were obtained from bacterial culture. H. pylor i genotype was determined by means of the polymerase chain reaction. The PM N oxidative burst in H. pylori infected patients was significantly higher t han that in H. pylori negative or healthy controls, no differences being fo und when the results following WEcagA+ and WEcagA- stimulation were compare d. The difference in PMN oxidative burst obtained after WEcagA- and E. coli (standard stimulus for PMN oxidative burst) stimulation discriminated H. p ylori infected from non-infected patients with a sensitivity of 90% and a s pecificity of 97%. The grade of PMN oxidative burst correlated with PMN inf iltration grade of the gastric mucosa. Our findings allow to conclude that PMN oxidative burst activation by H. pylori WE is species- but not strain-c orrelated. PMN priming, probably consequent to the action of soluble mediat ors released by mononuclear cells, makes PMN hyper-responsive to H. pylori products, thus favoring the release in the gastric mucosa of infected patie nts of large amounts of oxygen-derived free radicals, which are: not enough to eliminate the infection, but may contribute to damaging the gastric muc osa itself, peripheral PMN oxidative burst response to H. pylori WE might f urthermore be of help in diagnosing H. pylori infection.