Determination of markers of systemic inflammation is one of the important directions in the study of pathogenesis and improvement of diagnosis of chronic obstructive pulmonary disease (COPD), asthma-COPD overlap (ACO), and bronchial asthma (BA). The aim of our work was a comparative study of the features of changes in serum levels of IL-17, IL-18, and TNF-αin patients with COPD, ACO, and BA with various severity of the disease, as well as evaluation of the relationship between the level of these cytokines and lung ventilation function. A total of 147 patients with COPD (n=58), ACO (n=57), and BA (n=32) during a stable period have been examined in this study. The control group included 21 healthy nonsmokers with similar sex-age indicators. Serum levels of IL-17, IL-18, and TNF-αwere determined by ELISA. The concentrations of these cytokines in the circulation in the studied patients with COPD, ACO, and BA were higher than those in healthy nonsmokers (p≤0.001). IL-17 and IL-18 levels in the blood serum were comparable in all examined patients. The mean TNF-αconcentrations in the circulation in COPD and ACO were significantly higher than those in BA (p<0.001). In patients with COPD, the levels of IL-17 and TNF-αincreased progressively against the background of a decrease in numerous spirometric indicators, which allows us to consider these cytokines as systemic biomarkers of disease severity. In BA, the inverse correlations between the level of IL-17 and FEV1/FVC (%) and FEV1 have been found. In patients with ACO, the increase in IL-18 levels was associated with a decrease in FEV1 and TNF-αwith FEV1/FVC (%). These findings indicate that IL-17, IL-18, and TNF-αcan participate in the mechanisms of systemic inflammation and the genesis of disorders of airway obstruction in COPD, AСO, and BA. An increase in the levels of IL-17 and TNF-αmay be associated with impaired bronchial patency in COPD and BA. The established associations of the IL-18 concentration in the blood serum and FEV1 only in patients with ACO allow using the level of IL-18 as a potential marker of the degree of impaired airway obstruction in this disease.

In 43 patients aged 4–17 years with atopic BA and AR, the NM was examined using nasal video-endoscopy and (if indicated) computed tomography; the amount of periostin in the nasal secretion was determined by the enzyme immunoassay. Exacerbation of AR was accompanied by a statistically significant increase in the level of periostin in the nasal secretion: up to 0.84 [0.06; 48.79] ng/mg, whereas in remission, that was 0.13 [0.00; 0.36] ng/mg; p=0.04. This value increased progressively as the severity of AR increased from 0.16 [0.00; 0.36] ng/mg in the mild course to 0.20 [0.00; 9.03] ng/mg in AR of moderate severity, and to 10.70 [0.56; 769.20] ng/mg in most severe cases; p=0.048. Hypertrophy or polyposis of the nasal and/or paranasal mucosa was detected in 34.9% (15/43) of the examined patients. The concentration of periostin in the nasal secretion was lower in children without NM hypertrophy: 0.18 [0.001; 4.30] ng/mg vs 0.78 [0.13; 162.10] ng/mg in patients with NM hypertrophy; the differences were close to statistically significant: p=0.051. The level of nasal periostin depended on the clinical form of hypertrophy in the sinonasal mucosa, reaching 0.17 [0.00; 0.32] ng/mg in children with polyposis hyperplasia of NM and 21.6 [10.70; 1516.80] ng/mg — with hypertrophy of the NM in the medial surface of the concha; p=0.02. Exacerbation and increased severity of AR in patients with atopic BA are accompanied by an increased level of periostin in the nasal secretion. This allows us to consider the level of nasal periostin as a biomarker of local allergic inflammation in the NM of patients with atopic BA combined with AR. Hypertrophic changes in the sinonasal mucosa are generally accompanied by an increased level of nasal periostin; specifically, this level significantly depends on the clinical form of mucous membrane hypertrophy and requires additional studies.

Soluble molecules of the major histocompatibility complex play an important role in the development of various immune-mediated diseases. However, there is not much information on the participation of these proteins in the pathogenesis of chronic obstructive pulmonary disease (COPD). The aim of our work was to determine the content of soluble molecules of the major histocompatibility complex of classes I and II (sHLA-I and sHLA-II) in the exhaled breath condensate (EBC) and in the blood serum in patients with moderate to severe COPD during the exacerbation and stable phase. We investigated 105 patients (male) with COPD aged 46–67 and 21 healthy nonsmoking volunteers (male) comparable in age. The content of sHLA-I and sHLA-II molecules was studied using ELISA. We found an increase in the level of sHLA-I and sHLA-II molecules in EBC, as well as an enhancement in the serum content of sHLA-II in all the examined COPD patients compared to healthy nonsmoking volunteers. The revealed negative correlation between the serum concentration of sHLA-II and values of FEV₁ and FEV₁/FVC in all examined patients with COPD gives a possibility to consider the content of these proteins as an additional systemic marker of disease severity. The maximum endobronchial and serum concentrations of sHLA-I and sHLA-II were detected in patients with severe COPD during the exacerbation. The negative associations between the content of these molecules in EBC and serum and the parameters of lung function in patients with severe COPD were established. These findings suggest a pathogenetic role of sHLA-I and sHLA-II molecules in the mechanisms of the development and progression of local and systemic inflammation in COPD.

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The potential mechanisms of bronchial asthma (BA) negative modification under the influence of obesity are currently being actively studied. However, at present, the effect of nutritional status on bronchial obstruction in children with BA cannot be considered established. In this regard, the purpose of this work was to study the relationship of spirometric parameters reflecting bronchial patency with nutritional status in children with asthma. Materials and Methods. The study involved 54 patients with BA at the age of 8 to 17 years, 33 boys and 21 girls with different nutritional status. Assessment of nutritional status was carried out with the calculation of body mass index (BMI), relative body mass index (RBMI), and determination of body fat (% BF). Spirogram parameters were evaluated, including forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), FEV1/FVC ratio, maximum expiratory flow at the point of 25% loop flow-volume (MEF 25). Results. Among the children examined, taking into account the BMI Z-score, 9.3% (5/54) had low body weight (group 1), 33% (18/54) had normal body weight (group 2), 31.5% (17/54) overweight (group 3), 25.9% (14/54) obesity (group 4). As the body weight increased, a statistically significant decrease in the FEV1/FVC ratio was observed, amounting to 84.6 [79.3; 90.0], 79.4 [76.6; 82.2], 74.6 [71.7; 77.5], 70.2 [67.0; 73.4]%, respectively, p=0.003; as well as a decrease in MEF 25 (% pred.), which amounted, respectively, to 95.6 [76.1; 115.2], 81.7 [71.4; 92.0], 56.3 [45.7; 66.9], and 48.4 [36.7; 60.1]%, p=0.003. A statistically significant negative relationship was found between indicators of nutritional status, including BMI, RBMI, % BF, and spirometry parameters reflecting bronchial patency, including FEV1/FVC ratio and MEF 25 (% pred.); all p<0.01. Conclusions. Overweight and obesity in children with BA, estimated both by calculated methods with determination of BMI and RBMI and direct determination of body fat content, are accompanied by a statistically significant decrease in bronchial patency.