tetano
Editor, Senior Moderator
Front Immunol
. 2022 Nov 17;13:1016991.
doi: 10.3389/fimmu.2022.1016991. eCollection 2022.
Increased IL-26 associates with markers of hyperinflammation and tissue damage in patients with acute COVID-19
Eduardo I Cardenas[SUP] 1 [/SUP], Sandra Ekstedt[SUP] 2 [/SUP], Krzysztof Piersiala[SUP] 3 [/SUP], Marianne Petro[SUP] 2 [/SUP], Agneta Karlsson[SUP] 2 3 [/SUP], Åsa Kågedal[SUP] 2 3 [/SUP], Susanna Kumlien Georén[SUP] 2 [/SUP], Lars-Olaf Cardell[SUP] 2 3 [/SUP], Anders Lindén[SUP] 1 4 [/SUP]
Affiliations
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 TNFα, respectively. Moreover, the increase in blood IL-26 correlates with 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 correlates with that of increased lactate dehydrogenase, an established marker of tissue damage, and decreased mean 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.
Keywords: IL-26; IL-6; IL-8; TNF; cd47; coronavirus disease 2019 (COVID-19); neutrophils; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).
. 2022 Nov 17;13:1016991.
doi: 10.3389/fimmu.2022.1016991. eCollection 2022.
Increased IL-26 associates with markers of hyperinflammation and tissue damage in patients with acute COVID-19
Eduardo I Cardenas[SUP] 1 [/SUP], Sandra Ekstedt[SUP] 2 [/SUP], Krzysztof Piersiala[SUP] 3 [/SUP], Marianne Petro[SUP] 2 [/SUP], Agneta Karlsson[SUP] 2 3 [/SUP], Åsa Kågedal[SUP] 2 3 [/SUP], Susanna Kumlien Georén[SUP] 2 [/SUP], Lars-Olaf Cardell[SUP] 2 3 [/SUP], Anders Lindén[SUP] 1 4 [/SUP]
Affiliations
- PMID: 36466824
- PMCID: PMC9712219
- DOI: 10.3389/fimmu.2022.1016991
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 TNFα, respectively. Moreover, the increase in blood IL-26 correlates with 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 correlates with that of increased lactate dehydrogenase, an established marker of tissue damage, and decreased mean 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.
Keywords: IL-26; IL-6; IL-8; TNF; cd47; coronavirus disease 2019 (COVID-19); neutrophils; severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).