COVID-19 patients upregulate toll-like receptor 4-mediated inflammatory signaling that mimics bacterial sepsis

Observational studies of the ongoing coronavirus disease 2019 (COVID-19) outbreak suggest that a cytokine storm is involved in the pathogenesis of severe illness. However, the molecular mechanisms underlying the altered pathological inflammation in COVID-19 are largely unknown. We report here that t...

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Bibliographic Details
Published in:bioRxiv 2020-07
Main Authors: Kyung Mok Sohn, Sung-Gwon, Lee, Hyeon Ji Kim, Cheon, Shinhyea, Jeong, Hyeongseok, Lee, Jooyeon, In Soo Kim, Silwal, Prashanta, Young Jae Kim, Park, Chungoo, Kim, Yeon-Sook, Eun-Kyeong Jo
Format: Article
Language:English
Subjects:
Coronaviruses
COVID-19
Cytokine storm
Inflammation
Leukocytes (mononuclear)
Molecular modelling
Peripheral blood mononuclear cells
Sepsis
TLR4 protein
Toll-like receptors
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Summary:Observational studies of the ongoing coronavirus disease 2019 (COVID-19) outbreak suggest that a cytokine storm is involved in the pathogenesis of severe illness. However, the molecular mechanisms underlying the altered pathological inflammation in COVID-19 are largely unknown. We report here that toll-like receptor (TLR) 4-mediated inflammatory signaling molecules are upregulated in peripheral blood mononuclear cells (PBMCs) from COVID-19 patients, compared with healthy controls. Among the most highly increased inflammatory mediators in severe/critically ill patients, S100A9, an alarmin and TLR4 ligand, was found as a noteworthy biomarker, because it inversely correlated with the serum albumin levels. These data support a link between TLR4 signaling and pathological inflammation during COVID-19 and contribute to develop therapeutic approaches through targeting TLR4-mediated inflammation. Competing Interest Statement The authors have declared no competing interest.
DOI:10.1101/2020.07.17.207878