Basso D, Stefani A, Gallo N, Brigato L, Navaglia F, Toma A, Zancanaro F, Di Mario F, De Franchis G, Plebani M
Department of Laboratory Medicine, University of Padua, Italy.
Clin Chem Lab Med. 1999 Mar;37(3):223-9. doi: 10.1515/CCLM.1999.041.
H. pylori-associated gastric mucosal inflammation is characterized by the presence of polymorphonuclear (PMN) leukocyte infiltrate, which is more severe when the infecting strain is cagA positive. After appropriate stimuli, such as bacterial products, PMN release large amounts of oxygen derived free radicals and proteases, to kill the bacterium. H. pylori seems to be particularly resistant to the oxidative machinery of PMN, which can in turn damage the host gastric mucosa. We evaluated peripheral PMN oxidative burst response after stimulation with water extracts from cagA positive (WEcagA+) or negative (WEcagA-) H. pylori strains in infected (n=31) and non-infected patients (n=32) in comparison with healthy controls (n=16); the influence of gastric mucosal inflammatory infiltrate and activity grade on PMN oxidative burst were also assessed. PMN oxidative burst was measured by FACS analysis. H. pylori water extracts were obtained from bacterial culture. H. pylori genotype was determined by means of the polymerase chain reaction. The PMN oxidative burst in H. pylori infected patients was significantly higher than that in H. pylori negative or healthy controls, no differences being found when the results following WEcagA+ and WEcagA- stimulation were compared. The difference in PMN oxidative burst obtained after WEcagA- and E. coli (standard stimulus for PMN oxidative burst) stimulation discriminated H. pylori infected from non-infected patients with a sensitivity of 90% and a specificity of 97%. The grade of PMN oxidative burst correlated with PMN infiltration grade of the gastric mucosa. Our findings allow to conclude that PMN oxidative burst activation by H. pyloriWE is species- but not strain-correlated. PMN priming, probably consequent to the action of soluble mediators released by mononuclear cells, makes PMN hyper-responsive to H. pylori products, thus favoring the release in the gastric mucosa of infected patients of large amounts of oxygen-derived free radicals, which are not enough to eliminate the infection, but may contribute to damaging the gastric mucosa itself. Peripheral PMN oxidative burst response to H. pyloriWE might furthermore be of help in diagnosing H. pylori infection.
幽门螺杆菌相关的胃黏膜炎症的特征是存在多形核（PMN）白细胞浸润，当感染菌株为细胞毒素相关基因A（cagA）阳性时，炎症更为严重。在受到适当刺激后，如细菌产物，PMN会释放大量氧衍生自由基和蛋白酶来杀死细菌。幽门螺杆菌似乎对PMN的氧化机制具有特别的抗性，而这反过来又会损害宿主胃黏膜。我们评估了感染患者（n = 31）和未感染患者（n = 32）以及健康对照者（n = 16）在用cagA阳性（WEcagA +）或阴性（WEcagA -）幽门螺杆菌菌株的水提取物刺激后外周PMN的氧化爆发反应；还评估了胃黏膜炎症浸润和活动程度对PMN氧化爆发的影响。通过流式细胞术分析测量PMN氧化爆发。幽门螺杆菌水提取物从细菌培养物中获得。通过聚合酶链反应确定幽门螺杆菌基因型。幽门螺杆菌感染患者的PMN氧化爆发明显高于幽门螺杆菌阴性或健康对照者，比较WEcagA +和WEcagA -刺激后的结果时未发现差异。WEcagA -与大肠杆菌（PMN氧化爆发的标准刺激物）刺激后获得的PMN氧化爆发差异可区分幽门螺杆菌感染和未感染患者，灵敏度为90%，特异性为97%。PMN氧化爆发程度与胃黏膜PMN浸润程度相关。我们的研究结果表明，幽门螺杆菌水提取物激活PMN氧化爆发是种属相关而非菌株相关。PMN的致敏可能是单核细胞释放的可溶性介质作用的结果，使PMN对幽门螺杆菌产物反应过度，从而有利于感染患者胃黏膜中释放大量氧衍生自由基，这些自由基不足以消除感染，但可能有助于损害胃黏膜本身。此外，外周PMN对幽门螺杆菌水提取物的氧化爆发反应可能有助于诊断幽门螺杆菌感染。
