Zhang Q B, Nakashabendi I M, Mokhashi M S, Dawodu J B, Gemmell C G, Russell R I
Department of Gastroenterology, University of Glasgow NHS Trust.
Gut. 1996 Jun;38(6):841-5. doi: 10.1136/gut.38.6.841.
Helicobacter pylori is associated with neutrophil infiltration within the gastroduodenal mucosa. Neutrophil activation provides a major source of oxygen free radicals, which have been implicated in the pathogenesis of peptic ulceration.
To investigate if cytotoxin producing strains of H pylori are associated with the generation of oxidative burst in polymorphonuclear neutrophils (PMNs).
76 patients undergoing endoscopy of whom 45 had peptic ulcer and 31 chronic gastritis only were studied.
Strains of H pylori were cultured in Brucella broth. After 48 hours, bacteria were harvested by centrifugation and a bacterial suspension prepared as a stimulus for PMN oxidative burst using chemiluminescence. PMNs were prepared from health blood donors. To test the ability of strains to produce cytotoxin, culture supernatants of each were concentrated by polyethylene glycol and tested on cultured Vero cells for intracellular vacuolation.
30 of 45 (66.7%) peptic ulcer patients induced cell vacuolation versus nine of 31 (29%) strains from patients with chronic gastritis only (p < 0.01). Cytotoxin positive strains of H pylori regardless of the presence or absence of peptic ulcer displayed an increased induction of respiratory burst in PMNs compared with toxin negative strains from patients with chronic gastritis only (p < 0.05). Among the toxin negative strains, those from patients with peptic ulcer did not show a significant increase of the oxidative burst than those from patients without peptic ulcer (NS).
Toxinogenicity of strains of H pylori seems to be correlated with neutrophil respiratory burst and peptic ulceration. The ability of some strains of H pylori to produce cytotoxin and to induce the oxidative burst in neutrophils may be important in the pathogenesis of peptic ulcer disease.
幽门螺杆菌与胃十二指肠黏膜内的中性粒细胞浸润有关。中性粒细胞激活是氧自由基的主要来源,而氧自由基与消化性溃疡的发病机制有关。
研究产细胞毒素的幽门螺杆菌菌株是否与多形核中性粒细胞(PMN)氧化爆发的产生有关。
76例接受内镜检查的患者,其中45例患有消化性溃疡,31例仅患有慢性胃炎。
幽门螺杆菌菌株在布鲁氏菌肉汤中培养。48小时后,通过离心收集细菌,并制备细菌悬液作为PMN氧化爆发的刺激物,采用化学发光法检测。PMN取自健康献血者。为检测菌株产生细胞毒素的能力,各菌株的培养上清液用聚乙二醇浓缩,并在培养的Vero细胞上检测细胞内空泡形成情况。
45例消化性溃疡患者中有30例(66.7%)诱导细胞空泡形成,而仅患有慢性胃炎的31例患者中有9例(29%)菌株诱导细胞空泡形成(p<0.01)。与仅患有慢性胃炎患者的毒素阴性菌株相比,无论有无消化性溃疡,幽门螺杆菌细胞毒素阳性菌株在PMN中诱导呼吸爆发的能力均增强(p<0.05)。在毒素阴性菌株中,消化性溃疡患者的菌株与无消化性溃疡患者的菌株相比,氧化爆发无显著增加(无统计学意义)。
幽门螺杆菌菌株的产毒性似乎与中性粒细胞呼吸爆发和消化性溃疡有关。幽门螺杆菌某些菌株产生细胞毒素并诱导中性粒细胞氧化爆发的能力可能在消化性溃疡病的发病机制中起重要作用。