Russian MedicineRussian MedicineРоссийский медицинский журнал0869-21062412-9100Eco-Vector64291910.17816/medjrf642919MYIMTDOriginal Research ArticlesОригинальные исследованияResearch ArticleBronchial asthma and obesity: features of systemic inflammation depending on the time of asthma onsetБронхиальная астма и ожирение: особенности системного воспаления в зависимости от времени дебюта астмыhttps://orcid.org/0000-0002-1598-436X3045-8493AnikinDmitry А.АникинДмитрий Александрович
Russian Federation

MD

anikin27111994@mail.ruhttps://orcid.org/0000-0002-1999-95348713-5470SolovevaIrina A.СоловьеваИрина Анатольевна
Russian Federation

MD, Dr. Sci. (Medicine), Associate Professor

д-р мед. наук, доцент

acad-prorector@krasgmu.ruhttps://orcid.org/0000-0001-8982-52926520-3233DemkoIrina V.ДемкоИрина Владимировна
Russian Federation

MD, Dr. Sci. (Medicine), Professor

д-р мед. наук, профессор

demko64@mail.ruhttps://orcid.org/0000-0002-9377-52139132-6756SobkoElena A.СобкоЕлена Альбертовна
Russian Federation

MD, Dr. Sci. (Medicine), Professor

д-р мед. наук, профессор

sobko29@mail.ruhttps://orcid.org/0000-0002-0586-83497914-7630GordeevaNatalia V.ГордееваНаталья Владимировна
Russian Federation

MD, Cand. Sci. (Medicine), Associate Professor

канд. мед. наук, доцент

natagorday@yandex.ruhttps://orcid.org/0000-0001-6896-877X8829-9240KraposhinaAngelina Yu.КрапошинаАнгелина Юрьевна
Russian Federation

MD, Cand. Sci. (Medicine), Associate Professor

канд. мед. наук, доцент

angelina-maria@inbox.ruProfessor V.F. Voino-Yasenetsky Krasnoyarsk State Medical UniversityКрасноярский государственный медицинский университет имени профессора В.Ф. Войно-ЯсенецкогоKrasnoyarsk Clinical Regional HospitalКраевая клиническая больница, г. Красноярск28092025041120253154444571312202422082025Copyright ©; 2025, Eco-VectorCopyright ©; 2025, Эко-Вектор2025Eco-VectorЭко-Векторhttps://creativecommons.org/licenses/by-nc-nd/4.0/https://medjrf.com/0869-2106/article/view/642919

BACKGROUND: Bronchial asthma (asthma) is a complex, heterogeneous, multifactorial chronic disease. The pathophysiological mechanisms of the interaction between asthma and obesity have attracted considerable attention.

AIM: The work aimed to assess the characteristics of the cytokine profile in patients with asthma and obesity depending on the time of asthma onset.

METHODS: A total of 180 individuals were examined: 150 patients with asthma of varying severity were stratified by body mass index and divided into two study groups: those with a body mass index of 18.5–25 kg/m2 (n = 52, Asthma group) and those with a body mass index of 30–35 kg/m2 (n = 98). The control group consisted of 30 individuals. Patients with asthma and obesity (body mass index > 30 kg/m2) were further subdivided into two groups according to the time of asthma onset: Obesity + Asthma and Asthma + Obesity (with asthma duration of approximately 10 years). Asthma severity was assessed using the Asthma Control Test (ACT) and the Asthma Control Questionnaire (ACQ-5). Spirometry with bronchodilator testing was performed, and venous blood was collected to determine cytokine profile parameters (tumor necrosis factor-alpha; interleukins IL-2, IL-4, IL-6, IL-8, IL-10, IL-17; interferon-gamma) and markers of systemic inflammation (C-reactive protein, fibrinogen).

RESULTS: The asthma–obesity phenotype was characterized by a more severe course and poorer disease control, with the Obesity + Asthma group showing the most pronounced bronchial obstruction. Analysis of the cytokine profile revealed a significant imbalance between proinflammatory and anti-inflammatory cytokines, most pronounced in the Obesity + Asthma group. The findings underscore the importance of determining cytokine ratio indices with opposing activities (IL-2/IL-4, IL-2/IL-10, IL-8/IL-10, IL-6/IL-10, tumor necrosis factor-alpha/IL-10) to assess the severity of the inflammatory process and guide treatment strategies.

CONCLUSION: Obesity contributes to the development and maintenance of systemic inflammation, aggravating the course and progression of asthma.

Обоснование. Бронхиальная астма (БА) — сложное гетерогенное полиэтиологическое хроническое заболевание. Представляют интерес патофизиологические механизмы взаимодействия БА и ожирения.

Цель. Оценить особенности цитокинового профиля у больных БА в сочетании с ожирением в зависимости от времени дебюта астмы.

Методы. Обследовано 180 человек: 150 больных БА различной степени тяжести, разделённых с учётом индекса массы тела, составили две группы исследования: с индексом массы тела от 18,5 до 25 кг/м2 (n=52) — «БА»; с индексом массы тела от 30 до 35 кг/м2 (n=98). Группу контроля составили 30 человек. Далее пациенты с астмой в сочетании с ожирением (индекс массы тела >30 кг/м2) были разделены на две группы в зависимости от времени дебюта астмы: «Ожирение + БА»; «БА + ожирение» (с давностью БА около 10 лет). В процессе исследования оценивали степень тяжести БА с использованием теста по контролю над астмой (ACT) и опросника по контролю симптомов астмы (ACQ-5), проводили спирографию с бронхолитической пробой, выполняли забор венозной крови для определения показателей цитокинового профиля (фактора некроза опухоли альфа; интерлейкинов — ИЛ-2, 4, 6, 8, 10, 17; интерферона гамма), маркеров системного воспаления (С-реактивный белок, фибриноген).

Результаты. Фенотип БА в сочетании с ожирением характеризовался более тяжёлым течением и худшим контролем заболевания, причём в группе «Ожирение + БА» отмечались наиболее выраженные нарушения бронхиальной проходимости. При анализе цитокинового профиля в исследуемых группах был отмечен значимый дисбаланс провоспалительных и противовоспалительных цитокинов, наиболее выраженным он оказался в группе «Ожирение + БА». Полученные данные подчёркивают важность определения индекса соотношения цитокинов с противоположной активностью (ИЛ-2/ИЛ-4, ИЛ-2/ИЛ-10, ИЛ-8/ИЛ-10, ИЛ-6/ИЛ-10, фактор некроза опухоли альфа/ИЛ-10) для оценки степени выраженности воспалительного процесса и дальнейшей тактики лечения пациентов.

Заключение. Ожирение способствует формированию и поддержанию системного воспаления, усугубляя течение и прогрессирование БА.

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