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幽门螺杆菌对人吞噬细胞氧化代谢的激活作用。

Activation of human phagocyte oxidative metabolism by Helicobacter pylori.

作者信息

Nielsen H, Andersen L P

机构信息

Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.

出版信息

Gastroenterology. 1992 Dec;103(6):1747-53. doi: 10.1016/0016-5085(92)91430-c.

DOI:10.1016/0016-5085(92)91430-c
PMID:1451968
Abstract

A characteristic feature of chronic antral gastritis is the abundant inflammatory response in close association with Helicobacter pylori, but the immunopathological mechanisms of tissue damage are unknown. Because reactive oxygen radicals have been implicated in the tissue damage of other chronic inflammatory disorders, we investigated the potential ability of H. pylori sonicate to influence the oxidative burst responsiveness of human polymorphonuclear leukocytes and monocytes. For both cell types, a dose-dependent stimulation in a chemiluminescence system was observed. Furthermore, preincubation in sonicate caused a marked priming of the cells to subsequent stimulation with the oligopeptide N-f-methionyl-leucyl-phenylalanine and phorbol-myristate-acetate. The sonicate activity was nondialysable, completely destroyed by proteinase and resistant to heat treatment. However, dialysis of boiled sonicate significantly reduced the activity, suggesting the breakdown of a larger molecule(s) to smaller fragments still biologically active. Preliminary experiments suggest that the activity is 25-35 kilodaltons. The demonstration of a protein with stimulatory activity for production of reactive oxygen radicals by human phagocytes may contribute to the understanding of the immunopathology associated with H. pylori infection.

摘要

慢性胃窦炎的一个特征性表现是与幽门螺杆菌密切相关的丰富炎症反应,但组织损伤的免疫病理机制尚不清楚。由于活性氧自由基与其他慢性炎症性疾病的组织损伤有关,我们研究了幽门螺杆菌超声裂解物影响人多形核白细胞和单核细胞氧化爆发反应性的潜在能力。对于这两种细胞类型,在化学发光系统中观察到了剂量依赖性刺激。此外,在超声裂解物中预孵育导致细胞对随后用寡肽N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸和佛波醇肉豆蔻酸酯乙酸酯刺激产生明显的预激发作用。超声裂解物的活性不可透析,被蛋白酶完全破坏且耐热处理。然而,煮沸的超声裂解物透析后活性显著降低,这表明较大分子分解为仍具有生物活性的较小片段。初步实验表明该活性物质分子量为25 - 35千道尔顿。证明一种对人吞噬细胞产生活性氧自由基具有刺激活性的蛋白质可能有助于理解与幽门螺杆菌感染相关的免疫病理学。

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