Introduction. The high prevalence of asthma in the general population necessitates the assessment of medical students' theoretical knowledge regarding the pathogenesis, diagnosis, and management of this disease.

   Aim. To determine the level of basic knowledge among senior medical students across key thematic blocks of asthma.

   Materials and methods. The fourth stage of the multicenter study "The Assessment of Physicians' (Medical Students') Knowledge in the Field of Bronchial Asthma" (ASSA) was conducted between October 2023 and May 2025 using a validated, author-developed questionnaire based on current national and international clinical guidelines. The questionnaire consisted
of 21 questions divided into two blocks: "Etiopathogenesis" and "Pharmacotherapy".

   Results. A total of 487 correctly completed questionnaires from 5 universities of the Russian Federation were analyzed. The average rate of correct answers (ARC) for the entire questionnaire was 69.9 % (95 % CI 68.5–71.3 %), with a median (Me) of 70.6 % [IQR: 59.5%–82.5 %]. In the "Etiopathogenesis" section, the ARC reached 84.0% (95% CI 82.5–85.4 %), whereas in the "Pharmacotherapy" section it was only 59.3 % (95 % CI 57.6–61.0 %). The maximum ARC values were obtained for questions regarding asthma control levels (96.3 %) and the definition of the term "status asthmaticus" (92.6 %). Conversely, the minimum values were recorded for questions concerning sublingual immunotherapy for house dust mite allergies (16.2 %) and add-on therapy at the 4^th step of treatment (27.7%). Significant inter-center differences were revealed across the entire questionnaire (H (4) = 53.263, p < 0.001, ε2 = 0.102) and its individual sections. When compared with the previous stage (ASSA-III), a statistically significant improvement in the results was observed: the overall ARC increased by 3.9 % (69.9 % vs. 66.0 %, p < 0.001), though the effect size remained weak (r = 0.119; CLES = 0.568).

   Conclusion. Senior medical students demonstrated a proficient level of knowledge regarding the etiopathogenesis and diagnosis of asthma, whereas their understanding of its pharmacotherapy remains insufficient. The significant inter-center variability in the average rate of correct answers underscores the urgent need to standardize educational methods and strengthen practical training in asthma management and treatment selection.

Aim. To study computed tomography (CT) parameters in patients with bronchial asthma (BA) who have recovered from COVID-19-associated pneumonia. Materials and methods. In patients with mild persistent BA (n = 68, group 1) and moderate BA (n = 58, group 2), spirometry and body plethysmography parameters, as well as lung CT data in inspiratory and expiratory phases of breathing, were analyzed. Results. Spirometry analysis in groups 1 and 2 showed that the forced expiratory volume in 1 second (FEV₁) was 90.7 ± 1.5 and 72.4 ± 2.0% of predicted, respectively (p = 0.0001); the mean forced expiratory flow at 25–75% of forced vital capacity (FEF_25-75) was 65.3 ± 2.6 and 40.3 ± 1.8% of predicted, respectively (p = 0.0001). CT examination revealed significant differences in postexpiratory air content of both lungs (EAC2) – 69 (25; 381) and 637 (219; 1157) ml, respectively (p < 0.001). The difference in internal diameters of the B1 bronchus between inspiration and expiration (IDB₁-IDB_1exp) was 0.31 ± 0.08 and 0.56 ± 0.09 mm (p = 0.043); the difference in IDB₁₀-IDB_10exp was 0.87 ± 0.11 and 0.37 ± 0.08 mm, respectively (p = 0.001). Correlation analysis in both groups demonstrated a strong association of postexpiratory air content of both lungs (EAC2) with FEV₁/FVC ratio (r = 0.41; p = 0.006 and r = -0.38; p = 0.023) and patient age (r = 0.46; p = 0.002 and r = 0.39; p = 0.018), respectively. In group 2 patients, the internal diameter of the B₁ bronchus during expiration directly correlated with expiratory airway resistance Raw ex (Rs = 0.53; p = 0.005); furthermore, an association was observed between bronchial wall density (BWD₁₀) and FEF_25-75 (r = -0.44; p = 0.0003) and the airway response to a bronchodilator ΔFEV_1bd (Rs = 0.43; p = 0.002). Conclusion. In patients with BA who have recovered from COVID-19-associated pneumonia, functional and morphological changes of the respiratory system were identified, the severity of which increases in cases of moderate disease course and is accompanied by worsening lung function and alterations in the bronchial tree. Comprehensive functional and radiological monitoring of this patient category is necessary for timely detection and correction of post-pneumonic disorders.

   Aim. To analyze three-year overall survival and mortality structure in patients with chronic obstructive pulmonary disease (COPD) depending on the presence or absence of a history of COVID-19.

   Materials and methods. From 2021 to 2024, two groups of patients with COPD were under dynamic observation: Group 1 (n = 207) consisted of individuals with COPD who had previously suffered from COVID-19; Group 2 (n = 129) consisted of patients with COPD without a history of COVID-19. The follow-up checkpoints were: initial examination, and examinations at 1, 3, 6, 12, 24, and 36 months from the time of inclusion in the study. Statistical analysis was performed using STATISTICA 13.0 software.

   Results. During the observation period (36 months), the total number of deaths in both groups amounted to 22.4 %. It was revealed that 12-month survival did not differ significantly between the groups (p > 0.05), whereas 36-month survival in Group 1 was significantly lower than in Group 2 by 10.0 % (p < 0.05). The mean observation time in Group 1 was reduced by 2.5 months compared to Group 2 (p < 0.01). The maximum differences in survival levels between the groups were established in the 18–24 month period. Furthermore, it was found that a history of COVID-19 in patients with COPD increased the relative risk of death within 3 years by 1.75 times (p < 0.05). The structure of mortality did not differ significantly between the groups; the leading causes of death in both groups were heart diseases, neoplasms, and COPD.

   Conclusion. A history of COVID-19 in patients with COPD significantly reduces three-year survival rates and increases the risk of long-term mortality, indicating the need to optimize the dispensary monitoring program for this category of patients.

   Aim. To study the clinical and functional features and course of chronic obstructive pulmonary disease (COPD) depending on the presence or absence of atrial fibrillation (AF), establish the impact of AF on hemodynamic parameters and lung function in these patients, and evaluate the efficacy of an angiotensin receptor-neprilysin inhibitor (ARNI) in COPD patients with AF.

   Materials and methods. A total of 60 patients with COPD were examined (85.0 % male; mean age 67.2 ± 4.1 years). The patients were divided into two groups: Group 1 (n = 28) comprised individuals with concomitant permanent AF receiving ARNI (sacubitril/valsartan at a starting dose of 100 mg/day) as part of quadruple therapy; the Group 2 (n = 32) consisted of patients with preserved sinus rhythm. All enrolled subjects underwent comprehensive clinical, laboratory, and instrumental examination.

   Results. At hospitalization, patients in Group 1 exhibited a more severe course of COPD: lower forced expiratory volume in 1 second (FEV1; p < 0.05) and a higher frequency of annual exacerbations (p < 0.01). According to the modified Medical Research Council (mMRC) scale, they demonstrated pronounced dyspnea, and in the 6-minute walk test (6MWT), they covered the shortest distance (p < 0.05). At baseline, Group 1 showed significantly elevated levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) compared to Group 2 (p < 0.001), against the background of reduced glomerular filtration rate (GFR; p < 0.01) and more pronounced cardiac remodeling (p < 0.05). The inclusion of ARNI in quadruple therapy resulted in a significant increase in ejection fraction (EF) of both ventricles, reduction in intracardiac volumes (p < 0.01), decreased NT-proBNP levels (p < 0.001), and improved GFR (p < 0.05).

   Conclusion. The use of ARNI in COPD patients with concomitant AF contributes to a significant improvement in clinical status, accompanied by a reduction in dyspnea and increased exercise tolerance. In comorbid COPD and AF patients, inclusion of ARNI in standard medical therapy is advisable to improve hemodynamic parameters and reduce the risk of complications.

   Aim. To determine the clinical features of community-acquired pneumonia (CAP) caused by Klebsiella pneumoniae.

   Materials and methods. A single-center, consecutive, retrospective study was conducted involving 52 HIV-negative patients diagnosed with K. pneumoniae–associated CAP. Hierarchical cluster analysis was used to construct dendrograms.

   Results. Two age peaks of pneumonia incidence were identified: 30–39 years (23.1 %) and 50–59 years (21.2 %). Most patients were urban residents (80.8 %), and acute disease onset was documented in 84.6 % of cases. Systemic intoxication symptoms included fever (88.5 %), weakness (92.3 %), excessive sweating (28.8 %), reduced appetite (15.4 %), headache (9.6 %), and chills, weight loss, or dizziness (each in 7.7 % of patients). Respiratory symptoms: productive cough (100 %); difficult-to-expectorate sputum in 78.8 % (more common in women, ratio 1.3:1); dyspnea in 69.2 % (predominantly in men, ratio 1.4:1); chest pain (23.1 %); purulent sputum (19.2 %); hemoptysis (3.8 %). Auscultatory and percussory findings: harsh breath sounds in 78.8 % (more frequent in men, ratio 1.5:1); diminished breath sounds over the affected area (71.2 %); dullness to percussion over the lesion (61.5 %); dry crackles in 57.7 % (predominantly in men, ratio 1.5:1); moist crackles (23.1 %); vesicular (normal) breath sounds in 19.2 % (significantly more common in women, ratio 12:1).

   Conclusion. Current clinical presentation of K. pneumoniae–associated CAP is characterized by prominent systemic intoxication (weakness in 92.3 %, fever in 88.5 %) and universal presence of productive cough (100 %). Although respiratory insufficiency was diagnosed in 65.4 % of patients, the majority were in satisfactory general condition upon hospitalization, indicating a favorable prognosis. Significant gender-related differences were observed: men had significantly higher rates of dyspnea (p = 0.039), harsh breath sounds (p = 0.002), and dry crackles (p = 0.032). Women more commonly exhibited difficult sputum expectoration (p = 0.025) and preserved vesicular breath sounds (p < 0.001). These clinical and anamnestic distinctions may be used to refine diagnostic algorithms.

   Introduction. Over the past decade, Achromobacter xylosoxidans has emerged as a significant pathogen, demanding improved bacteriological diagnostic methods.

   Aim. To develop a method for identifying A. xylosoxidans that is accessible for routine bacteriological practice.

   Materials and methods. Two culture groups were established: an experimental group comprising 4 strains of A. xylosoxidans, and a comparison group including 33 strains belonging to 10 other species of non-fermenting Gram-negative bacteria (NFGNB) with similar phenotypic characteristics (Stenotrophomonas maltophilia, Acinetobacter baumannii, Pseudomonas aeruginosa, Pseudomonas putida, Pseudomonas stutzeri, Pseudomonas fluorescens, Chryseobacterium indologenes, Empedobacter brevis, Elizabethkingia meningoseptica, Burkholderia cepacia). Species identification was confirmed using both the Vitek 2 Compact 30 automated system and the Vitek MS mass spectrometer. A CO₂ incubator was used for bacterial culturing.

   Results. The developed method for identifying A. xylosoxidans is based on the phenomenon of mucoid growth of pure cultures on blood agar when incubated in a CO₂ atmosphere for 24–48 hours. The high diagnostic value of this feature for differentiating the pathogen from phenotypically similar microorganisms was experimentally substantiated. During testing, the target phenotypic marker was observed in all 4 strains of the experimental group (A. xylosoxidans) and was completely absent in all 33 isolates of the 10 other NFGNB species.

   Conclusion. The proposed methodological approach will optimize the bacteriological diagnosis of this difficult-to-identify and therefore rarely detected pathogen, thereby reducing the frequency of diagnostic errors across the wide spectrum of diseases it causes.

   Introduction. The development of postinfectious airway hyperresponsiveness in children remains a major challenge in pediatric pulmonology. Despite the accumulated clinical and functional data, molecular genetic predictors of this condition are still insufficiently studied.

   Aim. To investigate the frequency distribution of genotypes and alleles of the polymorphic loci of TRPV2 (rs1129235, rs3813769, rs7217735), TRPV4 (rs6606743), and TRPM8 (rs11562975) genes in children with various patterns of post-infectious airway reactivity to a hypoosmolar stimulus.

   Materials and methods. A total of 105 children aged 10 [8, 12] years were examined during the recovery phase of respiratory diseases. The mean height of the children was 148.7 ± 1.5 cm, body weight was 40 [30, 53] kg, and body mass index (BMI) was 17.4 [15.7, 20.4] kg/m². Airway response to a hypoosmolar stimulus was assessed using a bronchial provocation test with ultrasonic inhalation of distilled water (IDW). Genotyping of the polymorphic loci in TRPV2, TRPV4, and TRPM8 genes was performed by real-time polymerase chain reaction (qPCR) in peripheral blood leukocytes, followed by high-resolution melting (HRM) curve analysis. The mRNA expression levels of target genes in nasal epithelial cells were determined by quantitative reverse transcription PCR (RT-qPCR) in real-time.

   Results. Based on the results of the bronchial provocation test with IDW, the patients were divided into two groups: children with altered responsiveness to IDW (Group 1, n = 59) and children with no reaction to the stimulus (Group 2, n = 40). In Group 1 patients, airway dysfunction was verified at all levels of the bronchial tree, affecting the entire spectrum of expiratory flow parameters. Molecular genetic analysis revealed a highly significant protective effect of the overdominant inheritance model for the synonymous locus rs6606743 of the TRPV4 gene. It was established that the heterozygous AG genotype was associated with a 4-fold reduction in the odds of developing hypoosmolar bronchospasm in children (OR = 0.25; 95 % CI: 0.10–0.61; p = 0.002). According to the linear regression analysis performed on the entire cohort, the minor A allele of the rs6606743 SNP in the TRPV4 gene was associated with a statistically significant decrease in the degree of FEV₁ decline in response to IDW (β = +3.66 %, R² = 0.075, p = 0.0149). No statistically significant associations with the risk of pathology were found for the loci of the TRPM8 and TRPV2 genes.

   Conclusion. The data obtained confirm the contribution of genetic factors to the formation of post-infectious airway reactivity in children. The heterozygous AG genotype of the rs6606743 locus in the TRPV4 gene serves as an independent protective factor that reduces the odds of developing hypoosmolar bronchospasm, whereas the carriage of the minor A allele is associated with a stepwise decrease in the severity of bronchoconstriction. This polymorphism can be considered a prognostic marker for assessing the course of the post-infectious period of respiratory pathology in pediatric practice.

Introduction. Transient receptor potential channels TRPV1 and TRPV4 are expressed in leukocytes and may contribute to the pathogenesis of chronic obstructive pulmonary disease; however, data on their functional roles in immune cells remain limited and contradictory. Aim. To determine changes in the expression of surface activation markers on human peripheral blood lymphocytes and monocytes in response to pharmacological stimulation of TRPV1 and TRPV4. Materials and methods. Peripheral blood mononuclear cells were isolated from eight apparently healthy volunteers (39.9 ± 2.00 years; 50% male) by Ficoll density-gradient centrifugation. The effects of the TRPV1 agonist capsaicin and the TRPV4 agonist RN1747 on cell metabolic activity were assessed using the CCK-8 assay. The expression of the activation markers CD63, CD25, CD69, CD11b, and HLA-DR on lymphocytes and monocytes was evaluated by flow cytometry after 24 h of incubation with 10 μM capsaicin or 10 μM RN1747. Expression levels were reported as the percentage of positive cells or as normalized median fluorescence intensity (nMFI). Statistical significance was assessed using p values adjusted by the Benjamini–Hochberg method (padj). Results. Capsaicin and RN1747, each at 10 μM, did not reduce the metabolic activity of mononuclear cells. Capsaicin significantly decreased the proportions of monocytes positive for CD63 (79.19 [66.89; 86.55]% vs. 65.94 [56.45; 79.52]%, p_adj = 0.03), CD25 (12.81 [5.83; 18.47]% vs. 9.33 [5.51; 16.47]%, p_adj = 0.04), CD11b (95.06 [94.20; 96.92]% vs. 93.78 [91.89; 94.74]%, p_adj = 0.03), and CD69 (36.54 [34.42; 40.63]% vs. 29.65 [23.07; 33.94]%, p_adj = 0.03). Significant reductions in nMFI were observed for CD63 (3.39 [3.04; 3.86] vs. 2.86 [2.44; 3.17], p_adj = 0.01), CD25 (1.39 [1.30; 1.49] vs. 1.29 [1.18; 1.43], p_adj = 0.01), HLA-DR (36.87 [20.30; 47.17] vs. 29.63 [16.80; 33.43], p_adj = 0.01), and CD69 (2.11 [1.95; 2.25] vs. 1.91 [1.74; 2.07], p_adj = 0.01). In lymphocytes, capsaicin reduced the proportions of CD63-positive cells (4.66 [4.00; 6.90]% vs. 3.84 [3.27; 5.87]%, p_adj = 0.04) and CD69-positive cells (5.01 [3.27; 9.42]% vs. 4.81 [2.67; 8.04]%, p_adj = 0.04). In monocytes, RN1747 reduced the nMFI of CD63 (3.39 [3.04; 3.86] vs. 2.78 [2.64; 3.01], p_adj = 0.04) and CD69 (2.11 [1.95; 2.25] vs. 1.88 [1.75; 2.00], p_adj = 0.04), but had no significant effect on lymphocytes. Conclusion. Monocytes demonstrated broader phenotypic sensitivity to pharmacological activation of TRPV channels, particularly TRPV1, in comparison with lymphocytes. The combined decrease in the studied markers may indicate the development of a hyporeactive monocyte phenotype with potentially reduced secretory, adhesive, migratory, phagocytic, and antigen-presenting functions.  

   Introduction. Interleukin-4 (IL-4) is a key mediator of Th2 inflammation in asthma and is capable of profoundly altering the receptor profile of monocytes. However, data on the effect of IL-4 on the expression of the bitter taste receptor family (TAS2R) in circulating immune cells are currently lacking.

   Aim. To characterize the effect of recombinant IL-4 at physiologically and pathophysiologically relevant concentrations on the protein expression of TAS2R4, TAS2R5, TAS2R14, TAS2R20, TAS2R31, and TAS2R38 in subsets of monocytes and lymphocytes from the peripheral blood of healthy donors in vitro.

   Materials and methods. The study was performed on peripheral blood mononuclear cells from 10 healthy volunteers. The cells were incubated for 24 hours with recombinant IL-4 at concentrations of 0.1, 1, and 10 ng/ml. TAS2R expression was assessed by flow cytometry on a FACSCanto II with analysis of the proportion of TAS2R-positive cells and normalized median fluorescence intensity (nMFI). Page's test and Wilcoxon's test for related samples were used for statistical processing.

   Results. Under control conditions, all six studied receptors were detected in both monocytes and lymphocytes; however, their basal expression was significantly higher in monocytes. IL-4 exerted a pronounced dose-dependent inhibitory effect on TAS2R expression predominantly in monocytes. A monotonic downward trend was found for TAS2R4, TAS2R5, TAS2R14, and TAS2R38, while no significant changes were observed for TAS2R31. The most pronounced decrease in nMFI in monocytes was observed for TAS2R38, TAS2R14, and TAS2R5. TAS2R20 exhibited a biphasic response: an increase in the proportion of monocytes expressing TAS2R20 at the minimum dose of IL-4 was combined with a decrease in nMFI at 10 ng/ml. In lymphocytes, the effect of IL-4 was much less pronounced. Despite the presence of individual statistical trends, no biologically significant changes in TAS2R expression
were detected.

   Conclusion. In a pilot in vitro experiment, IL-4 was associated with a monotonic decrease in TAS2R expression in peripheral blood monocytes, with relative stability of TAS2R31 and minimal effect in lymphocytes. These data expand our understanding of the subpopulation- and receptor-specific influence of the Th2 cytokine environment on TAS2R-dependent immunoregulation and suggest that IL-4 may be a potential factor in reducing the chemosensory and antimicrobial readiness of myeloid cells in asthma.

   Introduction. Respiratory viruses are the primary trigger for asthma exacerbations, and their initial detection by the body depends on pattern recognition receptors (PRRs) of the mucosa. The upper respiratory tract is the first to contact both infection and cold air; however, the impact of local cooling on PRR expression in asthma patients remains unstudied.

   Aim. To evaluate changes in the gene expression of PRRs (TLR3, TLR7, TLR8, TLR9, DDX58/RIGI, IFIH1/MDA5, and DHX58/LGP2) at the messenger ribonucleic acid (mRNA) level in the nasal epithelium of asthma patients in response to local cooling, and to determine the relationship between PRR expression levels and the frequency of acute respiratory viral infection episodes.

   Materials and methods. A total of 48 individuals were examined, including 30 asthma patients (aged 39.0 [23.0; 50.0] years, 53.3 % male), predominantly with mild persistent asthma (50 %), and 18 individuals without chronic diseases, with the exception of allergic rhinitis (aged 40.0 [30.0; 49.0] years, 38.9 % male). Inferior turbinate epithelium was collected by brush biopsy before and after a 3-minute nasal inhalation of cold air (-20 ºC), followed by RNA extraction from the obtained samples. The assessment of PRR gene expression was performed using quantitative reverse transcription PCR (RT-qPCR).

   Results. The baseline PRR profile of the nasal epithelium was characterized by high expression of TLR3, DHX58/LGP2, and IFIH1/MDA5, with no differences found between the groups. Local cooling was not accompanied by any significant changes in the expression of the studied PRRs across all subjects. More frequent respiratory viral infections were associated with decreased DHX58/LGP2 (ρ = -0.45, p = 0.01) and IFIH1/MDA5 (ρ = -0.42, p = 0.02) expression.

   Conclusion. Asthma patients are not characterized by any specific features in the mRNA expression of the studied PRR genes in the nasal epithelium. Short-term local cooling of the nasal cavity does not lead to changes in the PRR profile, whereas more frequent respiratory viral infections are associated with reduced expression of IFIH1/MDA5 and DHX58/LGP2.

   Introduction. COVID-19-associated lung injury (COVID-19-ALI) is characterized by diffuse alveolar damage. The manifestation of long-term comorbid complications of this infection is particularly relevant in patients with type 2 diabetes mellitus (T2DM).

   Aim. To evaluate the association of hemostasis parameters with acute phase severity and the subsequent onset of comorbidities in patients with COVID-19-ALI and T2DM.

   Materials and methods. The study examined 108 hospitalized patients with COVID-19-ALI (52 patients without T2DM and 56 with concomitant T2DM), as well as 22 healthy volunteers comparable in age and sex. During a 36-month follow-up, the incidence of the following comorbidities was evaluated: arterial hypertension, chronic cerebral ischemia, hypo- and hyperthyroidism, cardiac arrhythmias, exertional angina, and obesity. Results. The combination of COVID-19-ALI and T2DM was associated with profound disorders of hemostasis and fibrinolysis. A model was developed to evaluate the probability of a severe acute phase based on a complex of coagulation parameters, D-dimer, and the FGB gene rs1800790 polymorphism (AUC
= 0.92). To assess the risk of long-term pathology onset at 36 months, an algorithm based on an isolated thrombin time parameter was proposed (AUC = 0.79).

   Conclusion. A pronounced imbalance of the blood coagulation system in COVID-19-ALI and T2DM is associated with acute status severity and long-term prognosis. The developed software is applicable for objectifying patient status upon admission and stratifying the risk of long-term outcomes.

Introduction. The combination of chronic obstructive pulmonary disease (COPD) and pulmonary tuberculosis (TB) is a clinically significant comorbidity. The role of αβ- and γδ-T-cell immunity in their isolated and combined course remains insufficiently studied. Aim. To establish features of the subpopulation composition of peripheral blood Tlymphocytes in isolated COPD, isolated TB, their combination, and in conditionally healthy individuals, as well as to identify associations between the T-cell profile and indicators of pulmonary ventilation function and systemic inflammation. Materials and methods. Using flow cytometry in 55 men (TB – 17, COPD – 16, TB + COPD – 8, control group – 14), the relative proportions of CD3⁺-, αβ- (CD3⁺TCRγδ^-), and γδ- (CD3⁺TCRγδ⁺) T-lymphocytes were determined; absolute counts (×10⁹/L) were calculated using a two-platform method based on complete blood count data. The Kruskal–Wallis test with Dunn's post-hoc test and Holm correction, Cliff's δ effect size, Spearman correlations with Benjamini–Hochberg correction, and sensitivity analysis with exclusion of two observations with extremely low relative CD3⁺ content in the TB + COPD group were used. Results. The relative counts of CD3⁺ T-lymphocytes differed significantly between groups (H = 24.1; p < 0.001): maximum in isolated TB (19.4%), minimum in TB + COPD (11.8%; Cliff's δ = 1.00 when compared with TB). The absolute counts of CD3⁺ T-lymphocytes confirmed these differences: 1.71 × 10⁹/L in TB versus 1.00 in TB + COPD and 0.95 in COPD (p = 0.002). The proportion of γδ T-lymphocytes within the CD3⁺ pool decreased in patients with bronchopulmonary pathology (2.1–3.2%) compared to controls (6.9%); significance was maintained for TB (p < 0.01) and COPD (p < 0.001). CD3⁺ T-cells positively correlated with the forced expiratory volume in 1 second to forced vital capacity ratio (FEV₁/FVC) (ρ = 0.60) and FEV₁ (ρ = 0.48), and negatively with smoking history (ρ = −0.54), neutrophil-to-lymphocyte ratio (NLR), and IL-1β (both ρ = −0.47); all differences persisted in the sensitivity analysis. Conclusion. Isolated TB was associated with elevated CD3⁺/αβ-T-cell counts, whereas COPD and TB + COPD were associated with their reduction and a selective deficit of γδ-T-cells. Shifts in the T-cell profile are linked to the severity of bronchial obstruction, smoking history, and systemic inflammation. This allows consideration of the T-cell profile as a potential immunological marker of the broncho-obstructive phenotype in TB; however, confirmation of causal relationships requires prospective studies. 

   Introduction. The inflammatory process in COVID-19 is accompanied by profound remodeling of lipid metabolism; however, the nature of alterations in the fatty acid profile in pregnant women with this pathology remains insufficiently studied, which determines the relevance of the present research.

   Aim. To characterize quantitative changes in the spectrum of minor saturated fatty acids (SFAs) in the erythrocyte membrane in women with moderate COVID-19 during the second trimester of gestation.

   Materials and methods. The study included 79 women in the second trimester of pregnancy. The main group comprised 39 patients with moderate COVID-19, while the control group consisted of 40 women who had not been infected with COVID-19 previously or at the time of examination. Peripheral blood erythrocytes served as the study material. Quantitative analysis of the individual SFA spectrum in the erythrocyte membrane was performed by gas chromatography.

   Results. In pregnant women with moderate COVID-19 during the second trimester, a statistically significant increase in the levels of capric acid (by 30 %, p < 0.001), lauric acid (by 46 %, p < 0.001), pentadecanoic acid (by 45 %, p < 0.001), and heptadecanoic acid (by 43 %, p < 0.001) was detected in the peripheral blood erythrocyte membrane, against the background of a decreased concentration of myristic acid (by 65 %, p < 0.001).

   Conclusion. For the first time, an imbalance of minor SFAs in the erythrocyte membrane was characterized in pregnant women with moderate COVID-19 during the second trimester. In our opinion, the accumulation of minor SFAs–capric, lauric, pentadecanoic, and heptadecanoic acids–reflects a compensatory response of the organism aimed at protecting cells against SARS-CoV-2 and reducing the level of the inflammatory process, whereas the decreased content of myristic acid indicates impairment of the structural and functional integrity of the erythrocyte membrane.

   Introduction. DiGeorge syndrome (22q11.2 deletion) is a genetic disorder characterized by wide phenotypic polymorphism. Its main manifestations include congenital heart defects, immunodeficiency due to thymic hypoplasia, and hypocalcemia resulting from parathyroid gland dysfunction. High variability of clinical combinations often masks the syndrome as transsyndromic comorbidity, substantially complicating its timely verification.

   Aim. To describe a clinical case of incomplete 22q11.2 deletion syndrome (DiGeorge syndrome) diagnosed in a 15-year-old patient with chronic nonspecific lung diseases, in order to familiarize physicians with the clinical features of the disease and current diagnostic capabilities.

   Materials and methods. A retrospective analysis of the medical record of a patient followed up at the Khabarovsk Branch of the Far Eastern Scientific Center of Physiology and Pathology of Respiration – Research Institute of Maternity and Child Protection was performed.

   Results. A rare genetic pathology – incomplete form of DiGeorge syndrome – is described. Disease manifestation occurred at the age of seven months. The clinical picture developed against the background of a congenital malformation of the respiratory organs and was characterized by a complicated pulmonological history (recurrent pneumonia, bronchial asthma). The patient was also diagnosed with thymic hypoplasia, selective immunoglobulin A deficiency, relative T-helper cell deficiency, and hypoparathyroidism. The diagnosis was verified only at the age of 15 years based on whole-genome sequencing results, which revealed a heterozygous deletion of the 22q11.2 region.

   Conclusion. This case report demonstrates the difficulty of timely detection of the incomplete form of DiGeorge syndrome in the absence of early molecular genetic screening.

   Neuroimmune mechanisms and their role in the pathogenesis of asthma have been actively discussed in the scientific literature in recent years. There is emerging evidence of a relationship between neurotrophic factors and lipid metabolism in asthma. Despite the significance of existing research, the literature is insufficient to support a neuro-immune-lipid model of asthma that defines the pathogenetic relationship between these three systems. Brain-derived neurotrophic factor (BDNF) is implicated in the pathogenesis of bronchial hyperreactivity and remodeling, integrating the neuroimmune mechanisms of asthma pathogenesis. Lipid metabolism disturbances in asthma, including an imbalance of proinflammatory and anti-inflammatory lipid mediators, as well as changes in sphingolipid and cholesterol levels in cell membranes, can influence the expression of BDNF and its receptor, which form the BDNF/TrkB signaling pathway. This allows us to consider the relationship between lipids and neurotrophins as a mechanism linking metabolic dysregulation with neuroimmune inflammation and airway remodeling in asthma. In this mechanism, lipids are considered to act as mediators modulating BDNF activity by activating signaling pathways that regulate BDNF gene transcription. Further research will help substantiate a unified neuro-immune-lipid model of asthma pathogenesis.

   Aim. To analyze current scientific data on the mechanisms of impaired blood oxygen transport function in pregnant women with COVID-19.

   Materials and methods. A systematic search and pathophysiological analysis of relevant literature in the PubMed, Google Scholar, and eLibrary databases for the period 2015–2026 was conducted using the keywords: pregnancy, COVID-19, SARS-CoV-2, hemic hypoxia, erythron, hemoglobin, cytokine storm, hepcidin, hypoxia-inducible factor (HIF). Based on the inclusion criteria, 47 publications were selected and reviewed in detail.

   Results. It was substantiated that gestational remodeling (physiological hemodilution and increased tissue oxygen demand) initially reduces the adaptive reserve of the oxygenation system. The key factor in the development of hemic hypoxia in COVID-19 was established to be complex, mediated damage to the erythron: cytokine-induced hepcidin-ferroportin blockade (anemia of inflammation), viral infection of erythroid precursor cells in the bone marrow, as well as membranopathy and hemolysis of mature erythrocytes driven by oxidative stress. The role of HIF-1α as a trigger of the vicious cycle of hypoxia and inflammation is described. These disturbances were shown to form a three-phase cascade (hyperinflammation → hemic hypoxia → thromboembolic complications), which manifests predominantly during infection in the third trimester of gestation, critically increasing the risk of severe obstetric and fetal complications.

   Conclusion. Impairment of blood oxygen transport function in pregnant women with COVID-19 is multifactorial, with the leading role belonging to functional and structural dysfunction of the erythron. Understanding the molecular mechanisms of this process substantiates the ineffectiveness of standard isolated iron therapy in anemia of inflammation. This necessitates the development of fundamentally new, comprehensive approaches to early diagnosis, pathogenetic therapy, and prevention of hemic hypoxia to reduce maternal and perinatal losses.