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S100A8 may govern hyper-inflammation in severe COVID-19.
Deguchi, Atsuko; Yamamoto, Tomoko; Shibata, Noriyuki; Maru, Yoshiro.
  • Deguchi A; Department of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
  • Yamamoto T; Division of Pathological Neuroscience, Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan.
  • Shibata N; Division of Pathological Neuroscience, Department of Pathology, Tokyo Women's Medical University, Tokyo, Japan.
  • Maru Y; Department of Pharmacology, Tokyo Women's Medical University, Tokyo, Japan.
FASEB J ; 35(9): e21798, 2021 09.
Article in English | MEDLINE | ID: covidwho-1334263
ABSTRACT
The coronavirus disease 2019 (COVID-19) pandemic threatens human species with mortality rate of roughly 2%. We can hardly predict the time of herd immunity against and end of COVID-19 with or without success of vaccine. One way to overcome the situation is to define what delineates disease severity and serves as a molecular target. The most successful analogy is found in BCR-ABL in chronic myeloid leukemia, which is the golden biomarker, and simultaneously, the most effective molecular target. We hypothesize that S100 calcium-binding protein A8 (S100A8) is one such molecule. The underlying evidence includes accumulating clinical information that S100A8 is upregulated in severe forms of COVID-19, pathological similarities of the affected lungs between COVID-19 and S100A8-induced acute respiratory distress syndrome (ARDS) model, homeostatic inflammation theory in which S100A8 is an endogenous ligand for endotoxin sensor Toll-like receptor 4/Myeloid differentiation protein-2 (TLR4/MD-2) and mediates hyper-inflammation even after elimination of endotoxin-producing extrinsic pathogens, analogous findings between COVID-19-associated ARDS and pre-metastatic lungs such as S100A8 upregulation, pulmonary recruitment of myeloid cells, increased vascular permeability, and activation coagulation cascade. A successful treatment in an animal COVID-19 model is given with a reagent capable of abrogating interaction between S100A8/S100A9 and TLR4. In this paper, we try to verify our hypothesis that S100A8 governs COVID-19-associated ARDS.
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Full text: Available Collection: International databases Database: MEDLINE Main subject: Respiratory Distress Syndrome / Calgranulin A / Pandemics / Cytokine Release Syndrome / SARS-CoV-2 / COVID-19 / Inflammation Type of study: Prognostic study Topics: Long Covid / Vaccines Language: English Journal: FASEB J Journal subject: Biology / Physiology Year: 2021 Document Type: Article Affiliation country: Fj.202101013

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Full text: Available Collection: International databases Database: MEDLINE Main subject: Respiratory Distress Syndrome / Calgranulin A / Pandemics / Cytokine Release Syndrome / SARS-CoV-2 / COVID-19 / Inflammation Type of study: Prognostic study Topics: Long Covid / Vaccines Language: English Journal: FASEB J Journal subject: Biology / Physiology Year: 2021 Document Type: Article Affiliation country: Fj.202101013