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Журнал "Гастроэнтерология" Том 60, №1, 2026

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Інтерлейкін-22 при гострому панкреатиті: коли цитопротекція стає ризиком

Авторы: Чуклін С.М., Чуклін С.С.
Медичний центр Святої Параскеви, м. Львів, Україна

Рубрики: Гастроэнтерология

Разделы: Клинические исследования

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Резюме

Актуальність. Гострий панкреатит (ГП) — тяжкий запальний стан, що характеризується передчасною активацією травних ферментів, ушкодженням ацинарних клітин і формуванням системних ускладнень. Інтерлейкін-22 (IL-22), представник родини IL-10, привертає дедалі більшу увагу як медіатор на перетині імунної регуляції та епітеліального захисту. Накопичені експериментальні дані свідчать про контекстуальну залежність його ефектів: залежно від стадії ГП та характеристик імунного мікросередовища IL-22 може реалізовувати як протективні, так і потенційно патогенні властивості. Матеріали та методи. У цьому огляді узагальнено результати експериментальних і клінічних досліджень, присвячених вивченню ролі IL-22 при ГП. Проаналізовано дані мишачих моделей, експериментів in vitro та клінічних когортних спостережень із фокусом на сигнальних механізмах, тканинозахисних і ушкоджувальних ефектах, а також трансляційному потенціалі IL-22 як терапевтичної мішені та біомаркера. Результати. IL-22 забезпечує цитопротекцію ацинарних клітин через активацію сигнальних шляхів STAT3 і AKT/mTOR, обмежує надмірну автофагію та індукує експресію антиапоптичних білків (Bcl-2, Bcl-xL). Цитокін також підтримує цілісність кишкового бар’єра шляхом індукції Reg3β/γ, зменшує ураження легень завдяки стримуванню нейтрофільного запалення та демонструє гепатопротекторні й ренопротекторні властивості. У пацієнтів із тяжким ГП підвищені сироваткові рівні IL-22 асоціюються з розвитком шлунково-кишкової недостатності та системних ускладнень, що підкреслює його потенційну прогностичну цінність як біомаркера. Водночас IL-22 характеризується функціональною амбівалентністю: за певних умов при легкому ГП він може посилювати некротичні зміни, тоді як тривала активація IL-22-залежних сигнальних каскадів асоціюється з фіброгенезом і канцерогенезом. Критичним компонентом підтримання гомеостазу є негативна регуляція через білок-зв’язувач IL-22 (IL-22BP). Перспективним напрямом доклінічних досліджень залишаються нанотерапевтичні підходи, спрямовані на підвищення стабільності та ефективності доставки IL-22. Висновки. IL-22 розглядається як перспективний терапевтичний кандидат і потенційний біомаркер при ГП. Рекомбінантний IL-22 та сучасні системи доставки можуть знижувати ризик ускладнень при тяжкому перебігу захворювання, тоді як визначення IL-22 у крові здатне поліпшити прогностичну стратифікацію. Водночас залишаються невирішеними питання безпеки, оптимального терапевтичного вікна та довгострокових ризиків. Для інтеграції IL-22 у підходи персоналізованої медицини при ГП потрібні масштабні, методологічно коректно спроєктовані клінічні випробування.

Background. Acute pancreatitis (AP) is a severe inflammatory disorder characterized by premature activation of digestive enzymes, acinar cell injury, and systemic complications. Interleukin-22 (IL-22), a cytokine of the IL-10 family, has emerged as a key mediator linking immune regulation with epithelial protection. Experimental data suggest that IL-22 exerts both protective and pathogenic effects depending on disease stage and immune context. Materials and methods. This review synthesizes findings from experimental and clinical studies on IL-22 in AP. Literature from murine models, in vitro studies, and patient cohorts was analyzed with a focus on signaling mechanisms, tissue-protective versus pathogenic roles, and translational potential as a therapeutic target and biomarker. Results. IL-22 protects acinar cells via STAT3 and AKT/mTOR signaling, inhibits excessive autophagy, and induces anti-apoptotic proteins (Bcl-2, Bcl-xL). It enhances intestinal barrier function through Reg3β/γ induction, mitigates lung injury by restraining neutrophilic inflammation, and shows potential hepatoprotective and renoprotective effects. Elevated serum IL-22 levels in patients with severe AP correlate with gastrointestinal failure and systemic complications, suggesting its potential prognostic value as a biomarker. However, IL-22 displays functional duality: in mild AP, it may worsen necrosis, while chronic activation of IL-22-dependent signaling cascades has been associated with fibrosis and tumorigenesis. Negative regulation through IL-22 binding protein is critical component in maintaining homeostasis. Preclinical nanotherapeutic approaches have improved IL-22 delivery and stability. Conclusions. IL-22 represents both a promising therapeutic target and a potential biomarker in AP. Recombinant IL-22 and advanced delivery platforms could reduce complications in severe disease, while IL-22 measurement may refine prognostic stratification. Nevertheless, challenges remain regarding safety, therapeutic windows, and long-term risks. Large-scale clinical studies are needed to establish IL-22 as a cornerstone of precision medicine in AP.


Ключевые слова

гострий панкреатит; інтерлейкін-22; цитокіни; передача сигналів; біомаркери

acute pancreatitis; interleukin-22; cytokines; signal transduction; biomarkers


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