Objective: to study the immunophenotype of the macrophage population and the mechanisms of their vectorial redistribution in fibrous cavernous pulmonary tuberculosis.Materials and methods. The material for the study was fragments of the fibrous cavern wall and pericavernous lung tissue of the dead or surgical patients diagnosed with fibrous cavernous tuberculosis (n = 163). All patients were divided into 2 main groups: patients with active bacteria excretion (MTB+, n = 84) and patients with clinical abacillation (MTB–, n = 79) for immunohistochemistry with a panel of markers for: macrophages and histiocytes – CD68; vascular growth factor A – VEGF-A; T-helpers – CD4, and T-cytotoxic lymphocytes – CD8.Results. Following the analysis of CD68 expression, the population heterogeneity of macrophages was revealed depending on the intensity of the cytoplasmic reaction, functional activity, localization and quantitative characteristics. Three groups were identified: highly active, moderately active and weakly active. Based on the reaction with vascular growth factor A, it was determined that VEGF+ cells correspond to weakly active CD68+ macrophages and are located on the border between the specific granulation tissue and fibrous layer as well as in the pericavernous zone and intact lung tissue with a statistically significant predominance in patients with MTB– (p < 0.05). Regardless of the scope of bacterial secretion, the number of VEGF+ cells in the lymphoid follicle zone directly correlates with that of CD68+ macrophages in the pericavernous zone (R = 0.68) and indirectly correlates with the number of diffusely scattered VEGF+ cells in the fibrous capsule (R = –0.75). In the meantime, CD68+/VEGF+ are visualized in the zone of CD8+ T-lymphocytes, and CD68+/VEGF- – in the zone of CD4+ cell clusters. Such correlation indicates the redistribution of macrophages into type 2, which has a remodeling effect on the surrounding tissues with the potentiating participation of lymphoid cells.
Introduction. Morphological data on SARS-CoV-2-associated heart damage and its mechanisms are rather limited. However, clinical and morphological features of myocardial lesions in COVID-19 patients have been described and include myocardial ischemia, acute coronary syndrome, and acute myocarditis. The prevailing features of myocardial lesions and their consequences are still controversial. The aim of our research was to evaluate the morphological features of myocardial lesions in patients with severe COVID-19, using routine histological examination and immunohistochemistry (CD45) to confirm myocardial inflam-matory infiltration. Materials and methods. We analyzed samples of the left ventricular myocardium obtained during autopsy examination of 48 patients with severe COVID-19 who died from SARS-CoV-2-associated pneumonia. We used histological description and immunohistochemical methods. Results. The results revealed several histopathological features of COVID-19-associated myocardial lesions, including acute ischemia (25% of cases) and mild inflammatory changes termed borderline myocarditis (18.75% of cases). Other significant findings in the myocardium included microcirculatory vessel thrombosis. Conclusion. The study confirms the existing data on damage to myocardium in severe COVID-19. However, further studies are warranted. It may contribute to the development of new management strategies for severe COVID-19 patients. Keywords: SARS-CoV-2, heart, ischemia, myocarditis
Aim. To describe the ultrastructural characteristics of the blood-air barrier (BAB) interstitium in fi brous cavernous pulmonary tuberculosis (FCT) in comparison with chronic nonspecifi c lung diseases (CNSLD).Materials and methods. The fragments of the pericavernal zone and lung tissue were taken for the study at the resection border from the dead or operated for CNSLD persons (n = 163), and the perifocal and boundary zone of lung tissue. 116 CNSLD patients were divided into 3 subgroups: 1) chronic lung abscess (n = 42); 2) bronchiectasis (n = 44); 3) lung cyst (n = 30). The lung fragments of 30 patients who died from pathology not associated with lung diseases (myocardial infarction, acute cerebrovascular accident) were used as a control group to compare the morphological parameters. The criteria for inclusion of patients in the study: age from 18 to 65 years, negative clinical and laboratory data on the presence of comorbid pathology (viral hepatitis B, C and HIV). For TEM, lung fragments 1×1×1 mm in size were cut out and fi xed in a 2.5% glutaraldehyde solution in phosphate buffer (pH = 7.2–7.4) and washed in 0.1 M phosphate buffer (pH = 7.4), followed by dehydration in alcohols of an ascending concentration and placing in a mixture of Epon and Araldite resins according to the scheme. Ultrathin sections were made with Reynolds staining. Viewing and photographing preparations was carried out on a PEM-100 transmission electron microscope (Ukraine) (magnifi cation range from ×1000 to ×30 000). Results. It was established that changes in BAB components in all groups had similar features in the form of severe interstitial fi brosis, the signs of endothelial cell degeneration and destruction of varying degrees of severity, as well as the heterogeneity of the endothelial and epithelial basement membranes.Conclusion. Ultrastructural changes in the BAB components of the removed lung part in patients with FCT and chronic nonspecifi c lung diseases are characterised by a polymorphism with prevailing dystrophic and destructive changes in the perifocal zone of infl ammation, and compensatory-adaptive processes on the peripheral, especially at the resection border.
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