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- Title
Increased IL-26 associates with markers of hyperinflammation and tissue damage in patients with acute COVID-19.
- Authors
Cardenas, Eduardo I.; Ekstedt, Sandra; Piersiala, Krzysztof; Petro, Marianne; Karlsson, Agneta; Kågedal, Åsa; Kumlien Georén, Susanna; Cardell, Lars-Olaf; Lindén, Anders
- Abstract
Interleukin-26 (IL-26) is released by several immune and structural cells following stimulation of toll-like receptors (TLRs), whereupon it can directly inhibit viral replication and enhance neutrophil chemotaxis. Given these unique properties, IL- 26 has emerged as an intriguing mediator of host defense in the lungs. However, the role of IL-26 in COVID-19 has not been thoroughly investigated. Here, we characterized the involvement of IL-26 in the hyperinflammation and tissue damage that occurs in patients with acute COVID-19. We found that IL-26 is markedly increased in blood samples from these patients, and that the concentration of IL-26 correlates with those of the neutrophil-mobilizing cytokines IL-8 and TNFa, respectively.Moreover, the increase in blood IL-26 correlateswith enhanced surface expression of the "don't eat me" signal CD47 on blood neutrophils isolated from patients with acute COVID-19. Finally, we found that the blood concentration of IL-26 correlateswith that of increased lactate dehydrogenase, an established marker of tissue damage, and decreasedmean corpuscular hemoglobin (MCH), a previously verified hematological aberration in COVID-19, both of which are associated with severe disease. Thus, our findings indicate that increased systemic IL-26 associates with markers of hyperinflammation and tissue damage in patients with acute COVID-19, thereby forwarding the kinocidin IL-26 as a potential target for diagnosis, monitoring, and therapy in this deadly disease.
- Subjects
COVID-19; SARS-CoV-2; INFLAMMATION
- Publication
Frontiers in Immunology, 2022, Vol 13, p01
- ISSN
1664-3224
- Publication type
Article
- DOI
10.3389/fimmu.2022.1016991