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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.

Background: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary autosomal dominant vascular injury of the brain. Currently, the clinical diagnosis of CADASIL is based on the following criteria: the onset of the condition at a relatively young age (4050 years), recurrent lacunar infarcts, gradual progression of encephalopathy with the development of pseudobulbar syndrome and dementia, various emotional disorders, and autosomal dominant inheritance. Having a family history of relatives with similar symptoms. The diagnosis is verified on the basis of the results of the following studies: neuroimaging, instrumental, morphological, and laboratory. The presence of leukoaraiosis and multiple small bilateral infarctions in such anatomical structures as the basal ganglia and white matter of the cerebral hemispheres, visual tubercles and the pons, and brain stem during MRI diagnostics. Histologically, transmission electron microscopy reveals granular osmiophilic inclusions in the adventitial membrane of the blood vessels of the brain, and on the periphery in the adventitia of the vessels of skeletal muscles and somatic nerves and in vascular biopsies of skin flaps. A mutation in the Notch3 gene determines the clinic of the disease and morphological changes in blood vessels and is detected by a molecular genetic method. The article presents a clinical case, which was a manifestation of this rare hereditary microangiopathy. Clinical case description: A 43-year-old patient was admitted to the Department of Neurology of the Republican Clinical Hospital in Simferopol for ischemic stroke in the basin of the left middle cerebral artery. According to the anamnesis, the patient suffered from migraine without aura from a young age and lacunar strokes; examination revealed a decrease in cognitive function, and MRI showed signs of microangiopathy of cerebral vessels. For final diagnosis, the patient underwent an intravital pathomorphological examination of the biopsy of the musculoskeletal flap; the results obtained made it possible to make a reliable diagnosis of CADASIL. Conclusion: Understanding and knowledge of such a rare pathology as CADASIL is crucial for the rapid recognition of a characteristic clinical picture for further appointment and interpretation of the results of morphological and molecular genetic diagnostics, making it possible to make the correct diagnosis and treatment.

Background. Despite the progress and development of scientific directions in various fields of medicine, the problem of tuberculosis and its morphological manifestations remains relevant and is not fully disclosed due to complex pathogenesis, the presence of various clinical forms, therapeutic pathomorphosis, torpid to therapy, the presence of relapses. It is known that a surfactant system occupies a special place in the system of local lung protection.Aim. To study the condition of surfactant-assotiated protein A in the foci of specific destruction and in the surrounding intact lung tissue to assess its functional status, degree of respiratory failure and possible dissemination of tuberculous inflammation.Material and Metods. An analysis of 163 lung fragments of the dead or operated on for cavernous pulmonary tuberculosis with active bacterial excretion of 89 fragments and with clinical abacilation – 74 was carried out. Results A morphological study revealed stereotypical dynamic depression of surfactant-associated protein A in all the samples studied, both in the areas of cavernous destruction and pericavernouse zone, and in intact lung tissue. The maximum intensivity of the immunohistochemical expression of this surfactant protein was recorded in the alveolar macrophages, which indicated intensive recycling and utilization of the components of the surfactant.Conclusion. Minimizing the production of surfactant components and its active utilization in intact lung tissue leads to a collapse of the alveoli with subsequent progression of respiratory failure.

Background. It is well known that viral infections are able to cause an imbalance of the interferon system and inhibition of cellular and phagocytic reactions of the body. One of the possible solutions of the flu treatment problem may be the application of immunomodulators of native plant origin since the influenza virus possesses a suppressive effect on cellular immunity and the interferon system.The aim. To evaluate the effect of saponin tauroside Sx1 obtained from Crimean ivy leaves on histological changes in the spleen of mice infected with influenza A/WSN/1/33(H1N1) virus.Material and methods. We used 78 male BALB/c mice weighing 16–18 g which were divided into the groups: control (K; n = 12); healthy animals treated with saponin (KS; n = 22); animals infected with influenza virus A/WSN/1/33(H1N1) (V; n = 22); infected animals treated with saponin tauroside Sx1 twice a day for 3 days (SV; n = 22). Histological studies of the spleen were performed on the 4th (subgroups V, SV, KS) and 14th day (2V, 2SV, 2KS).Results. The spleen tissue of the KS subgroup demonstrated hyperplasia of the white pulp in the form of lymphoid nodules expansion. On the 4th day in the KS subgroup a statistically significant increase in the total area of the lymphoid nodules by 3.9 times compared to the K subgroup was observed. In subgroup V, there was a sharp decrease in the area of white pulp and in 2V the lymphoid nodules zones were practically indistinguishable. Applied correction in the SV and 2SV subgroups significantly ceased the damaging effect of the virus: the lymphoid nodules area increased by 2.7 times in the 2SV subgroup compared to 2V.Conclusion. Infection with the H1N1 influenza virus leads to compensatory activation of the immune response, however, on the 14th day, a pronounced depletion of the splenic white pulp occurred. The introduction of saponin tauroside Sx1 enhanced the functional activity of the spleen due to an increase of the white pulp area.