Division of Lung and Airway Research, Institute of Environmental Medicine, and the Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden.
Division of Ear, Nose and Throat Diseases, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden.
Front Immunol. 2024 Oct 4;15:1434186. doi: 10.3389/fimmu.2024.1434186. eCollection 2024.
IL-26 is a key mediator of pulmonary host defense given its abundant expression in human airways and its established antibacterial properties. Moreover, recent studies indicate that IL-26 can also inhibit viral replication. Along these lines, we have previously reported an increase in the plasma concentration of IL-26 among patients with acute COVID-19 that is linked to harmful hyperinflammation. Nevertheless, it is still unclear whether this systemic increase in IL-26 relates to disease severity, sex, comorbidities, viral load, or the innate immune response in acute COVID-19.
IL-26 was quantified using ELISA in plasma samples from a large cohort of well-characterized patients with acute COVID-19 (n=178) and healthy controls (n=30). The plasma concentrations of SARS-CoV-2 nucleocapsid and spike protein, as well as those of IFN-α2a, IFN-β, and IFN-γ, were determined using electrochemiluminescence immunoassay. The concentration of double-stranded DNA was determined using fluorometry.
The plasma concentration of IL-26 was increased in patients with severe/critical COVID-19, particularly among males and patients with comorbid obstructive lung disease. Moreover, the concentration of IL-26 displayed positive correlations with length of hospital stay, as well as with systemic markers of viral load, antiviral immunity, and extracellular DNA.
Systemic IL-26 is involved in severe COVID-19, especially in males and patients with comorbid obstructive lung disease. These findings argue that systemic IL-26 has pathogenic and antiviral relevance, as well as biomarker potential.
IL-26 是肺部宿主防御的关键介质，因为它在人体气道中大量表达，并具有已确立的抗菌特性。此外，最近的研究表明，IL-26 还可以抑制病毒复制。基于这些原因，我们之前报告了急性 COVID-19 患者血浆中 IL-26 浓度的增加，这与有害的过度炎症有关。然而，目前尚不清楚这种系统性增加的 IL-26 是否与疾病严重程度、性别、合并症、病毒载量或急性 COVID-19 中的固有免疫反应有关。
使用 ELISA 定量检测了来自大量特征明确的急性 COVID-19 患者（n=178）和健康对照者（n=30）的血浆样本中的 IL-26。使用电化学发光免疫测定法测定 SARS-CoV-2 核衣壳和刺突蛋白的血浆浓度，以及 IFN-α2a、IFN-β 和 IFN-γ 的浓度。使用荧光法测定双链 DNA 的浓度。
严重/危重症 COVID-19 患者的血浆 IL-26 浓度升高，尤其是男性和合并阻塞性肺疾病的患者。此外，IL-26 浓度与住院时间长短以及病毒载量、抗病毒免疫和细胞外 DNA 的全身标志物呈正相关。
系统性 IL-26 参与严重的 COVID-19，特别是在男性和合并阻塞性肺疾病的患者中。这些发现表明系统性 IL-26 具有致病性和抗病毒相关性以及生物标志物潜力。
