IL-26 in the Lung and Its Role in COPD Inflammation

Abstract

IL-26 is a cytokine expressed by infiltrating pro-inflammatory IL-17-producing T cells in the tissues of patients with chronic lung inflammation. IL-26 induces the chemotactic response of human neutrophils to bacteria and other inflammatory stimuli. In recent years, the innovative properties of IL-26 have been described. Studies have shown that, as DNA is released from damaged cells, it binds to IL-26, which plays the role of a carrier molecule for extracellular DNA, further contributing to its binding to the site of inflammation. This mechanism of action indicates that IL-26 may serve both as a driver as well as a stimulus of the inflammatory process, leading to the installation of a noxious amplification loop and, eventually, persistent inflammation. IL-26 also demonstrates direct antimicrobial effects derived from its capability to create pores and disrupt bacterial membranes, as indicated by the presence of membrane blebs on the surface of the bacteria and cytosolic leakage pores in bacterial walls, produced in response to microbial stimuli in human airways by several different immune and structural cells. Surprisingly, while this particular cytokine induces the gathering of neutrophils in areas of infection, it also exhibits inhibitory and pro-inflammatory effects on airway epithelial and immune cells. These remarkable effects underline the necessity of a better understating of its biological behavior and its role in the pathophysiology and disease burden in several smoking-related airway inflammatory disorders, such as Chronic Obstructive Pulmonary Disease (COPD) and chronic bronchitis. In this review, we aim to discuss the current role of IL-26 in the lung, with an emphasis on systemic inflammation in patients suffering from COPD and chronic bronchitis.

Current Views on the Role of the Pro-Inflammatory Cytokine IL-26 in the Development and Clinical Course of Bronchial Asthma Associated with Obesity and Treatment Strategy

“…Дослідження показали, що коли ДНК вивільняється з пошкоджених клітин, вона зв'язується з IL-26, який грає роль молекули-носія для позаклітинної ДНК, додатково сприяючи її зв'язуванню на місці запалення. Цей механізм дії вказує на те, що ІL-26 може служити як драйвером, так і стимулом запального процесу дихальних шляхів [29]. Аналіз експресії IL-26 при тяжкій формі БА як у периферичній крові, так і в індукованому мокротинні показав, що концентрації IL-26 вищі у сироватці крові та індукованому мокротинні пацієнтів з БА, ніж у групі контролю.…”

Interleukin 26 Induces Macrophage IL-9 Expression in Rheumatoid Arthritis

“…Previous studies reported that IL-26 was found to associate with many proinflammatory cytokines, such as IL-6, IL-10, IL-17A, TNF-α, and mediated recruitment of T help cells [ 10 , 12 , 13 ]. Besides RA, recent studies reported that IL-26 was also found in many inflammatory lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD) [ 14 ]. Even in the recent COVID-19 pandemic, IL-26 was regard as a marker of acute hyperinflammation [ 15 ].…”