Department of Pathophysiology, Bogomolets National Medical University, 01601 Kyiv, Ukraine.
Department of Internal Medicine, Corewell Health William Beaumont University Hospital, Royal Oak, MI 48073, USA.
Medicina (Kaunas). 2023 Apr 6;59(4):714. doi: 10.3390/medicina59040714.
The coronavirus (SARS-CoV-2) damages all systems and organs. Yet, to a greater extent, the lungs are particularly involved, due to the formation of diffuse exudative inflammation in the form of acute respiratory distress syndrome (ARDS) with next progression to pulmonary fibrosis. SARS-associated lung damage is accompanied by the pronounced activation of mononuclear cells, damage of the alveoli and microvessels, and the development of organized pneumonia. To study the expression of macrophage markers (CD68 and CD163), angiotensin-converting enzyme-2 (ACE2), and caspase-3 on the results of two fatal clinical observations of COVID-19. In both clinical cases, the female patients died from complications of confirmed COVID-19. Conventional morphological and immunohistochemical methods were used. There was an acute exudative hemorrhagic pneumonia with the formation of hyaline membranes, focal organization of fibrin, stromal sclerosis, stasis, and thrombus formation in the lung vessels. Signs such as the formation of hyaline membranes, organization, and fibrosis were more pronounced in severe disease activity. The activation of CD68+/CD163+ macrophages could cause cell damage at an early stage of pneumonia development, and subsequently cause fibrotic changes in lung tissue. ACE2 expression in lung tissue was not detected in severe pneumonia, while in moderate pneumonia, weak expression was noted in individual cells of the alveolar epithelium and vascular endothelium. This finding could show the dependence of ACE2 expression on the severity of the inflammatory process in the lungs. The expression of caspase-3 was more pronounced in severe pneumonia.
冠状病毒（SARS-CoV-2）会损害所有系统和器官。然而，由于弥漫性渗出性炎症以急性呼吸窘迫综合征（ARDS）的形式形成，随后发展为肺纤维化，肺部受到的影响更大。与 SARS 相关的肺部损伤伴随着单核细胞的显著激活、肺泡和微血管的损伤以及机化性肺炎的发展。为了研究巨噬细胞标志物（CD68 和 CD163）、血管紧张素转换酶 2（ACE2）和半胱氨酸蛋白酶-3 在 2 例 COVID-19 致命临床观察结果中的表达。在这 2 例临床病例中，女性患者均因确诊 COVID-19 的并发症而死亡。采用常规形态学和免疫组织化学方法。肺组织中存在急性渗出性出血性肺炎，形成透明膜，局灶性纤维蛋白组织，基质硬化，停滞和血管内血栓形成。在严重疾病活动期，透明膜形成、组织化和纤维化等迹象更为明显。CD68+/CD163+巨噬细胞的激活可能导致肺炎发展早期的细胞损伤，随后导致肺组织纤维化改变。在严重肺炎中未检测到肺组织中 ACE2 的表达，而在中度肺炎中，仅在肺泡上皮和血管内皮的个别细胞中观察到弱表达。这一发现表明 ACE2 的表达依赖于肺部炎症过程的严重程度。半胱氨酸蛋白酶-3 在严重肺炎中的表达更为明显。
