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ORIGINAL RESEARCH article

Front. Immunol.
Sec. Viral Immunology
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1434186
This article is part of the Research Topic Changes in T cell populations and cytokine production in SARS-CoV-2 infected individuals; their role in prognosis View all 19 articles

Systemic increase in IL-26 is associated with severe COVID-19 and comorbid obstructive lung disease

Provisionally accepted
Eduardo I. Cardenas Eduardo I. Cardenas 1,2*Josefina Robertson Josefina Robertson 3,4Salvia Misaghian Salvia Misaghian 5Jermaine Brown Jermaine Brown 5Mingyue Wang Mingyue Wang 5Martin Stengelin Martin Stengelin 5George Sigal George Sigal 5Jacob Wohlstadter Jacob Wohlstadter 5Magnus Gisslen Magnus Gisslen 3,4,6Anders Lindén Anders Lindén 1,7
  • 1 Division of Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Stockholm, Sweden
  • 2 Division of Ear, Nose and Throat Diseases, Department of Clinical Science, Intervention and Technology, Karolinska Institutet (KI), Stockholm, Stockholm, Sweden
  • 3 Department of Infectious Diseases, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
  • 4 Sahlgrenska University Hospital, Gothenburg, Sweden
  • 5 Meso Scale Diagnostics LLC, Rockville, Maryland, United States
  • 6 Public Health Agency of Sweden, Solna, Stockholm, Sweden
  • 7 Karolinska Severe COPD Center, Department of Respiratory Medicine and Allergy, Karolinska University Hospital, Stockholm, Stockholm, Sweden

The final, formatted version of the article will be published soon.

    Background: 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. Methods: 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. Results: 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. Conclusions: 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.

    Keywords: IL-26, COVID-19, SARS-CoV-2, Asthma, COPD. (Min.5-Max. 8)

    Received: 17 May 2024; Accepted: 17 Sep 2024.

    Copyright: © 2024 Cardenas, Robertson, Misaghian, Brown, Wang, Stengelin, Sigal, Wohlstadter, Gisslen and Lindén. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Eduardo I. Cardenas, Division of Lung and Airway Research, Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Stockholm, Sweden

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