ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021
S100A8 may govern hyper-inflammation in severe COVID-19.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Immune dysregulation in prolonged Long-COVID: lymphocytes emerge as key mediators of persistent inflammation, exhaustion and cytotoxicity.Journal of translational medicine · 2026Article
- The inflammation-immunosuppression loop as a driver of immune dysfunction and secondary infections in severe COVID-19.Frontiers in immunology · 2026Review
- LeLISA: A New Lectin-Based Immunoassay for Evaluation of Mucinous and Serous Content in Pancreatic Cystic Neoplasms.Digestive diseases and sciences · 2025Article
- An exploratory study on the metagenomic and proteomic characterization of hypothyroidism in the first half of pregnancy and correlation with Th1/Th2 balance.Frontiers in immunology · 2025Article
- Lung-Brain Axis-Generated Inflammatory Biomarkers in Traumatic Brain Injury and Acute Respiratory Distress Syndrome: Role of Mechanical Ventilation/Stress.Advances in biomarker sciences and technology · 2025Article
- Neutrophil gene expression in COVID-19 patients with acute respiratory distress syndrome.Frontiers in immunology · 2025Article
- Epigenetic training of human bronchial epithelium cells by repeated rhinovirus infections.Allergy · 2024Article
- IFN-American journal of respiratory cell and molecular biology · 2023Article
- Review
- Circulating Calprotectin as a Predictive and Severity Biomarker in Patients with COVID-19.Diagnostics (Basel, Switzerland) · 2022Article
- Characterization of Early Peripheral Immune Responses in Patients with Sepsis and Septic Shock.Biomedicines · 2022Article
- Dok3 restrains neutrophil production of calprotectin during TLR4 sensing of SARS-CoV-2 spike protein.Frontiers in immunology · 2022Article
- Role of myeloid-derived suppressor cells in viral respiratory infections; Hints for discovering therapeutic targets for COVID-19.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- S100A8 may govern hyper-inflammation in severe COVID-19.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
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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