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[单核吞噬细胞结构、代谢及功能紊乱在干酪性肺炎发病机制中的作用及意义]

[Role and significance of structural, metabolic and functional disorders of mononuclear phagocytes in pathogenesis of caseous pneumonia].

作者信息

Mishin V Iu, Khomenko A G, Koval'chuk L V, Pavliuk A S, Voronina G A, Puzanov V A

出版信息

Probl Tuberk. 1997(6):32-6.

PMID:9503928
Abstract

Comprehensive clinical, X-ray, cytochemical, morphological, biochemical, and immunological studies of 14 patients with caseous pneumonia have provided evidence that significant structural, metabolic, and functional disorders of mononuclear phagocytes (MNP) play a leading role in the pathogenesis of acute tuberculosis. Structural and metabolic disorders of macrophages and monocytes in patients with caseous pneumonia result from impaired mitochondrial oxidation and glycolysis, aggregation and latinization of the membranes of lysosomes, release of their contents into the cytosol with damages to intracellular structures and the cellular membrane itself. This is also suggested by a drastic rise in the production of prostaglandins E2 and F2 alpha, prostaglandins E2 in particular, in the supernatants of cultured monocytes (100 nM). This is determined as the membrane-damaging effect of MNP due to the toxic action of rapidly multiplying mycobacterial population not only in the lung, but even in blood. MNP structural and metabolic disturbances are an equivalent to their lowered functional activity, as evidenced by a considerable deficiency of synthesis of intracellular and secretory pools of interleukin I and by a fall in their migrational and adhesive activities, two thirds of macrophages having signs of dystrophy and cytolysis. On entering the specific inflammatory area of the lung, these cells abundantly disintegrate. Their destruction leads to the elaboration of enzymes, prostaglandins, and other biologically active agents, which promotes the occurrence of extensive caseously destructive changes and creates conditions for rapid multiplication of mycobacteria.

摘要

对14例干酪性肺炎患者进行的全面临床、X线、细胞化学、形态学、生化及免疫学研究表明,单核吞噬细胞(MNP)明显的结构、代谢和功能紊乱在急性结核病发病机制中起主导作用。干酪性肺炎患者巨噬细胞和单核细胞的结构及代谢紊乱是由线粒体氧化和糖酵解受损、溶酶体膜聚集和拉丁化、其内容物释放到细胞质中导致细胞内结构和细胞膜本身受损所致。培养单核细胞上清液中前列腺素E2和F2α尤其是前列腺素E2的产量急剧增加也表明了这一点(100 nM)。这被确定为MNP的膜损伤效应,这是由于快速繁殖的结核菌群不仅在肺部甚至在血液中的毒性作用。MNP的结构和代谢紊乱等同于其功能活性降低,这表现为白细胞介素I细胞内和分泌池合成明显不足,以及其迁移和黏附活性下降,三分之二的巨噬细胞有营养不良和细胞溶解的迹象。这些细胞进入肺部特定炎症区域后大量解体。它们的破坏导致酶、前列腺素和其他生物活性剂的释放,这促进了广泛的干酪样破坏性变化的发生,并为结核杆菌的快速繁殖创造了条件。

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