Bartziokas Konstantinos, Fouka Evangelia, Loukides Stelios, Steiropoulos Paschalis, Bakakos Petros, Papaioannou Andriana I
Pulmonologist, 42100 Trikala, Greece.
Respiratory Medicine Department, George Papanikolaou Hospital, University of Thessaloniki, 57010 Thessaloniki, Greece.
J Pers Med. 2022 Oct 9;12(10):1685. doi: 10.3390/jpm12101685.
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.
白细胞介素-26（IL-26）是一种由慢性肺部炎症患者组织中浸润的促炎产白细胞介素-17的T细胞所表达的细胞因子。IL-26可诱导人类中性粒细胞对细菌及其他炎症刺激产生趋化反应。近年来，IL-26的创新特性已被描述。研究表明，当DNA从受损细胞中释放出来时，它会与IL-26结合，IL-26作为细胞外DNA的载体分子发挥作用，进一步促进其与炎症部位的结合。这种作用机制表明，IL-26可能既是炎症过程的驱动因素，也是炎症刺激因素，导致有害的放大循环的形成，并最终导致持续性炎症。IL-26还表现出直接的抗菌作用，这源于其能够形成孔道并破坏细菌膜，在人类气道中，几种不同的免疫细胞和结构细胞对微生物刺激作出反应后，细菌表面出现的膜泡以及细菌细胞壁中的胞质渗漏孔就表明了这一点。令人惊讶的是，虽然这种特定的细胞因子会诱导中性粒细胞在感染区域聚集，但它对气道上皮细胞和免疫细胞也表现出抑制和促炎作用。这些显著的作用凸显了更好地了解其生物学行为及其在几种与吸烟相关的气道炎症性疾病（如慢性阻塞性肺疾病（COPD）和慢性支气管炎）的病理生理学和疾病负担中所起作用的必要性。在本综述中，我们旨在讨论IL-26在肺部的当前作用，重点关注COPD和慢性支气管炎患者的全身炎症。
