1 -Федеральное государственное бюджетное научное учреждение «Дальневосточный научный центр физиологии и патологии дыхания»: 675000, Благовещенск, ул. Калинина, 22; 2 -Федеральное государственное бюджетное образовательное учреждение высшего образования «Амурская государственная медицинская академия» Министерства здравоохранения Российской Федерации: 675013, Благовещенск, ул. Горького, 95 РезюмеПерсистенция воспаления дыхательных путей у больных бронхиальной астмой (БА) способствует развитию тяжелого неконтролируемо го течения болезни. Цель. Изучение особенностей воспалительных паттернов и клинико функциональных параметров тяжелой неконт ролируемой БА. Материалы и методы. В холодный период года (ноябрь -март) проведено обследование больных (n = 25) в возрасте от 45 до 55 лет с установленным диагнозом тяжелой неконтролируемой БА при помощи определения реактивности дыхательных путей на хо лодовой стимул по данным анамнестического тестирования, исследования функции внешнего дыхания по стандартной методике, цито логического и цитохимического исследования индуцированной мокроты (ИМ). Результаты. По данным анализа цитограмм ИМ больные были разделены на 2 группы: 1 я (n = 11) -с эозинофильным (> 2 % эозинофилов), 2 я (n = 14) -со смешанным (≥ 2 % эозинофилов + ≥ 61 % нейтрофилов) паттернами воспаления. Оксидативная функция лейкоцитов, оцениваемая по уровню миелопероксидазы в клет ках, степени деструкции и интенсивности цитолиза, доминировала во 2 й группе. У пациентов этой группы выявлены более выраженные симптомы и большее число случаев обострения БА, тенденция к снижению уровня контроля над болезнью по вопроснику Asthma Control Test, более значимое снижение максимальной объемной скорости в момент выдоха 25, 50 и 75 % форсированной жизненной емкости лег ких соответственно. Холодовая гиперреактивность дыхательных путей (ХГДП) по клинически значимым признакам установлена у боль ных 2 й (n = 12) и 1 й (n = 3) групп. Показано, что проявления тяжести течения болезни, нарушения вентиляционной функции легких и частота развития ХГДП у больных тяжелой неконтролируемой БА сопряжены с паттерном воспаления бронхов. Заключение. Смешан ный воспалительный паттерн связан с утяжелением течения БА и более сложной проблемой контроля над болезнью. Ключевые слова: тяжелая неконтролируемая бронхиальная астма, холодовая гиперреактивность дыхательных путей, паттерны вос паления бронхов. AbstractThe aim of this study was to investigate airway inflammation patterns and clinical and functional features of severe uncontrolled asthma. Methods. The study involved 25 patients aged 45 to 55 years with severe uncontrolled asthma. Medical history was analyzed. Lung function tests, cytological and cytochemical investigation of induced sputum were performed in all patients. Asthma control was assessed using the Asthma Control Test ques tionnaire. Results. The patients were divided into groups: with eosinophilic (> 2% of eosinophils; n = 11) or mixed (≥ 2% of eosinophils and ≥ 61% of neutrophils; n = 14) airway inflammation patterns according to induced s...

Destruction of bronchial epithelium in patients with bronchial asthma (BA) is at the bottom of the mechanism of epithelial dysfunction, mucociliary insufficiency and bronchial remodeling. The aim of the work is to assess the character of changes that happen in the structural organization of cell elements and secretory activity of bronchial goblet epithelium in response to cold bronchial challenge in BA patients with cold airway hyperresponsiveness (CAHR). 28 patients with mild BA took part in the research. In the first day of the research the collection of the induced sputum was done, then the next day there was conducted a standard 3-minute test of isocapnic hyperventilation with cold (-20ºC) air (IHCA), after that the collection of sputum was done again. In cytograms of the sputum the percentage, the degree of destruction and cytolysis intensity of cell elements was determined; the contents of glycoproteins in goblet epithelial cells (GS) was studied. The first group included 14 patients with CAHR, the group of comparison (the 2nd group) included 14 patients with BA who did not have airway response to IHCA (ΔFEV1=-19.9±1.6 and -2.8±1.3%, respectively, p=0.00001). After IHCA in cytograms of the sputum of the patients with CAHR there was an increase of the number of neutrophils in relation to the basic one (from 39.9±2.8 till 54.0±2.3%, respectively, p=0.0004), the decrease of the number of macrophages (from 45.3±3.4 till 31.4±2.6%, p=0.005) without the changes of the number of eosinophils (10.0±2.2 and 10.4±1.6%, p=0.14) against intensified cytolysis (2.4±0.16 and 3.1±0.16%, p=0.0007). There was a decrease of the number of GC in relation to the initial one (from 0.22±0.02 till 0.16±0.02%; p=0.037) without significant changes of the number of epithelial cells (1.6±0.54 and 1.5±1.20%; p=0.97). The total index of destruction of GC was 0.45±0.02 and 0.51±0.02 (p=0.045); the index of cytolysis intensiveness of GC was 0.20±0.04 and 0.20±0.02 (p=0.27). A high number of GC that had a normal structure (0 and 1 class of destruction) as well as an increase of the number of cells in relation to initial values of the number of cells of II class against the absence of changes of III and IV classes of destruction were quite noticeable. Under cytochemical reaction the number of alcian blue stained GC actively synthesizing and secreting glycoproteins in response to IHCA increased in relation to the basic value (from 59.8±3.3 till 70.8±4.0%, p=0.0002, respectively). There was found a close correlation between the intensified production of GC glycoproteins in response to bronchial challenge and intensification of bronchial response (∆FEV1) to IHCA (r=-0.37; p=0.029). Thus, in the patients with BA and CAHR a short-term cold air exposure leads to the increase of the number of neutrophils and the decrease of the number of GC under intensive production of glycoproteins in them.

The parameters of several populations of immune cells (T cell populations, macrophage subpopulations) in peripheral blood and brain were studied in a clinically significant model of mild traumatic brain injury among rats. The population of resident cells of innate immunity of microglia and brain astrocytes with local tissue damage is involved in the implementation of the inflammatory response, it is also shown that in case of trauma, blood leukocytes can overcome the blood-brain barrier and penetrate the brain parenchyma. The methods of flow cytometry and immunofluorescence were used. An increase in the number of monocytes and neutrophils up to 1 day, after a mild traumatic brain injury (TBI) with a subsequent decrease to the end of the observation period was noticed. It was determined, that the number of CD45+ cells, CD3+T cells decreased at 1 days post-injury (dpi), and rose slightly by 14 dpi, the percentage of CD4+T cells continuously declined from 7 to 14 dpi, while the percentage of CD8+T cells increased from 7 to 14 dpi. With mild traumatic brain injury in animals, a significant (3-10 times) decrease in the number of microvessels with a positive reaction to the presence of SMI 71 on the 8th and 14th day after head injury was observed. Intensive staining of SMI 71 microvessels was sometimes observed with an increase in the area of a positive reaction. Thin positive deposits of the reaction product are observed in the brain of healthy animals around the wall of the microvessel. In the damaged brain, CD45high/CD11b+ positive macrophages of the M1 subpopulation appeared in the brain tissue on the 2nd day after TBI and a significant amount was observed on the 8-14th day. In the corpus callosum and ipsilateral region of the striatum, the content of cells expressing CD16/11b+ reached a maximum 8 days after TBI, which correlated with a decrease in the positive response to the presence of endothelial antigen SMI 71. Thus, in the acute period of mild TBI, the presence of neuroimmunopathological processes is determined in the brain, which can subsequently result to the dysregulation of neuroimmune connections.