Pneumonia is the most common and deadly nosology among all respiratory diseases associated with microorganisms. Despite advances in antibacterial and antiviral therapy, mortality due to pneumonia is not decreasing. It should be noted that the problem of infectious pathology has always been discussed only in narrow circles of specialists, which led to its underestimation, including during the pandemic of a new coronavirus infection. At present, scientific possibilities have not reached their perfection in the etiological diagnosis of pneumonia. Of no small concern is the lack of sections on immunology in the training program for general practitioners and pulmonologists and, as a result, the lack of knowledge by most medical specialists of the basics of the immune response in various infectious diseases, in particular, the differences in the immune response of a macroorganism in viral and bacterial infections, the stages of the immune response, differences between innate and adaptive immune responses, possibilities of immunocorrective therapy. Being followers of the scientific school of pulmonology of academician N.S. Molchanov, in this review, we evaluated the features of etiological factors and immune characteristics of the body on the course and out-comes of pneumonia, taking into account modern scientific knowledge. The current definition of pneumonia is formulated, the issues of the etiology of pneumonia from the perspective of the lung microbiome, the features of the immune response of the macroorganism in viral and bacterial pneumonia, the inconsistency of immune protection and the impact of comorbidity on this are covered in detail. Understanding the processes that lead to the disruption of the respiratory microbiome, the multiplication of pathobionts, the attachment of multiresistant microorganisms and the reactivity of the macroorganism will contribute to the development of new therapeutic approaches in the treatment of pneumonia.
Intriduction. In the last decade, conflicting data has appeared that the presence of obesity in patients with several diseases not only does not worsen, but even improves their prognosis, which is called the “obesity paradox”. The role of elevated body mass index in patients with coronavirus pneumonia (COVID-19) remains unclear.Aim. To study the features of the course of pneumonia in young and middle-aged men depending on the body mass index.Materials and methods. A retrospective analysis has investigated and it included 451 young and middle-aged men who underwent inpatient treatment for COVID-19 pneumonia. Patients were randomized according to body mass index into groups: normal nutrition (N), overnutrition (On), obesity (Ob). Clinical and laboratory parameters were assessed using statistical analysis.Results and discussion. In patients with obesity, the causative agent of pneumonia was detected in 91.9% of cases, in contrast to group N (65.75%). At the onset of pneumonia, group Ob differed significantly from group N in terms of erythrocyte sedimentation rate (17 versus 9 mm/h), C-reactive protein (18.3 versus 7.2 mg/l), D-dimer (304 versus 230 ng/ml), glycemia (6.2 versus 5.2 mmol/l), lymphocytes 9 (1.3 versus 1.5 × 109/l). In the dynamics in the group Ob, in comparison with the group N, there is a higher level of platelets (307 versus 1 × 109/l), neutrophils (6.3 versus 3.7 × 109/l), monocytes (0.8 versus 0.6 × 109/l) and a smaller number of lymphocytes (1.4 versus 2.0 × 109/l). It was revealed that the lymphocytic index and the index of the ratio of lymphocytes to monocytes in dynamics significantly increase in group N (from 0.5 to 0.7 and from 3.5 to 4.5, respectively), in group On only the lymphocyte index significantly increases (from 0.4 to 0.5), in the obesity group they do not change (from 0.4 to 0.5 and 3 from.0 to 2.7, respectively). The greatest need for respiratory support had group Ob (21.1%) in comparison with GNP (6.0%).Conclusions. The level of adipose tissue in the body has a direct impact on the course of pneumonia.
BACKGROUND: When studying new and effective methods of treating acute respiratory distress syndrome, an immunogenic model of lung injury occupies a special place. To date, the search for the optimal strategy and regimen for the use of glucocorticoids in the development of acute respiratory distress syndromе is relevant. AIM: The article evaluates the effectiveness of various schemes of systemic anti-inflammatory therapy with glucocorticoids in an experimental model of acute LPS-induced lung injury. MATERIALS AND METHODS: The study was conducted on 100 outbred male rats. Acute lung injury was modeled using an experimental model of direct acute lung injury by a single intratracheal injection of lipopolysaccharide (LPS) from the cell wall of the bacterium Salmonella enterica (Sigma-Aldrich) at a dose of LD50 (20 mg/kg). All animals were divided into groups (20 each): 1 intact rats; 2 control group (LPS + saline); 3 LPS + dexamethasone 0.52 mg/kg (small doses); 4 LPS + dexamethasone 1.71 mg/kg (average doses); 5 LPS + dexamethasone 8 mg/kg (high doses). The drugs were administered intraperitoneally once a day for 3 days. Dexamethasone doses were calculated using the interspecies dose transfer method using a factor that takes into account differences in body surface area. RESULTS: It has been established that an experimental model based on the endotracheal administration of S. enterica leads to the development of mortality from pulmonary causes. According to a preclinical study, the systemic use of low doses of dexamethasone (0.52 mg/kg) was found to be better than higher doses (1.71 mg/kg, 8 mg/kg) in the treatment of acute LPS-induced lung injury.
CHF6001 is a new inhaled phosphodiesterase-4 inhibitor that is safe and well tolerated by both healthy people and patients with bronchial asthma. The effect of CHF6001, in addition to standard triple therapy for chronic obstructive pulmonary disease, was evaluated on some inflammatory markers in induced sputum and blood in 61 patients (54 completed the study) with chronic obstructive pulmonary disease and chronic bronchitis. From October 2016 to November 2017, a multicenter, three-period (every 32 days), tripartite, placebo-controlled, double-blind, complete block cross-sectional study was conducted in Great Britain and Germany. Patients were treated by CHF6001 at doses of 800 or 1600 g, or the corresponding placebo using the dry powder inhaler NEXThaler. The induced sputum was collected on day 1 before the treatment and days 20, 26, and 32 after the treatment. Blood was also collected on day 1 before the treatment and day 32 before and after the treatment. Result analyses took into account the inflammatory biomarkers in induced sputum and blood, respiratory function, and symptoms and side effects. CHF6001, which supplements triple therapy in patients with moderate to severe chronic obstructive pulmonary disease and chronic bronchitis, was well tolerated and significantly reduces the number of key biomarkers of airway inflammation in sputum and blood after 32 days of treatment. CHF6001, administered by inhalation, creates a high therapeutic concentration in the lungs compared with other systemic phosphodiesterase-4 inhibitors and improves the therapeutic index due to anti-inflammatory effects while minimizing the possible side effects typical of the latter.
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