Discrimination of COVID-19 From Inflammation-Induced Cytokine Storm Syndromes Using Disease-Related Blood Biomarkers.


Journal

Arthritis & rheumatology (Hoboken, N.J.)
ISSN: 2326-5205
Titre abrégé: Arthritis Rheumatol
Pays: United States
ID NLM: 101623795

Informations de publication

Date de publication:
10 2021
Historique:
received: 20 11 2020
accepted: 06 04 2021
pubmed: 22 4 2021
medline: 13 10 2021
entrez: 21 4 2021
Statut: ppublish

Résumé

Infection with the novel coronavirus SARS-CoV-2 triggers severe illness with high mortality in a subgroup of patients. Such a critical course of COVID-19 is thought to be associated with the development of cytokine storm, a condition seen in macrophage activation syndrome (MAS) and secondary hemophagocytic lymphohistiocytosis (HLH). However, specific data demonstrating a clear association of cytokine storm with severe COVID-19 are still lacking. The aim of this study was to directly address whether immune activation in COVID-19 does indeed mimic the conditions found in these classic cytokine storm syndromes. Levels of 22 biomarkers were quantified in serum samples from patients with COVID-19 (n = 30 patients, n = 83 longitudinal samples in total), patients with secondary HLH/MAS (n = 50), and healthy controls (n = 9). Measurements were performed using bead array assays and single-marker enzyme-linked immunosorbent assay. Serum biomarker levels were assessed for correlations with disease outcome. In patients with secondary HLH/MAS, we observed pronounced activation of the interleukin-18 (IL-18)-interferon-γ axis, increased serum levels of IL-1 receptor antagonist, intercellular adhesion molecule 1, and IL-8, and strongly reduced levels of soluble Fas ligand in the course of SARS-CoV-2 infection. These observations appeared to discriminate immune dysregulation in critical COVID-19 from the well-recognized characteristics of other cytokine storm syndromes. Serum biomarker profiles clearly separate COVID-19 from MAS or secondary HLH in terms of distinguishing the severe systemic hyperinflammation that occurs following SARS-CoV-2 infection. These findings could be useful in determining the efficacy of drugs targeting key molecules and pathways specifically associated with systemic cytokine storm conditions in the treatment of COVID-19.

Identifiants

pubmed: 33880885
doi: 10.1002/art.41763
pmc: PMC8251089
doi:

Substances chimiques

Biomarkers 0
Interleukin-18 0
Interleukin-8 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1791-1799

Subventions

Organisme : European Union's Horizon 2020 research and innovation program
ID : 779295
Organisme : Deutsche Forschungsgemeinschaft
ID : FO 354/14-1

Informations de copyright

© 2021 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology.

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Auteurs

Christoph Kessel (C)

Department of Pediatric Rheumatology and Immunology, University Children's Hospital Muenster, Muenster, Germany.

Richard Vollenberg (R)

Department of Gastroenterology, Hepatology, Endocrinology and Clinical Infectiology, University Hospital Muenster, Muenster, Germany.

Katja Masjosthusmann (K)

Department of General Pediatrics, University Children's Hospital Muenster, Muenster, Germany.

Claas Hinze (C)

Department of Pediatric Rheumatology and Immunology, University Children's Hospital Muenster, Muenster, Germany.

Helmut Wittkowski (H)

Department of Pediatric Rheumatology and Immunology, University Children's Hospital Muenster, Muenster, Germany.

France Debaugnies (F)

Laboratory of Translational Research, Centre Hospitalier Universitaire Brugmann, Université Libre de Bruxelles, Brussels, Belgium and Medical Biology Department, Laboratoire National de Santé, Dudelange, Luxembourg.

Carole Nagant (C)

Immunology Department, LHUB-ULB, Université Libre de Bruxelles, Brussels, Belgium.

Francis Corazza (F)

Laboratory of Translational Research, Centre Hospitalier Universitaire Brugmann and Immunology Department, LHUB-ULB, Université Libre de Bruxelles, Brussels, Belgium.

Frédéric Vély (F)

Aix Marseille Université, CNRS, INSERM, CIML and Assistance Publique des Hôpitaux de Marseille, Hôpital de la Timone, Immunology, Marseille Immunopole, Marseilles, France.

Gilles Kaplanski (G)

Assistance Publique-Hôpitaux de Marseille, Centre Hospitalier Universitaire Conception, Service de Médecine Interne et Immunologie Clinique, Aix-Marseille Universitô and Center for Cardiovascular Research and Nutrition, Aix-Marseille Université, INSERM UMRS1263, Marseilles, France.

Charlotte Girard-Guyonvarc'h (C)

Division of Rheumatology, Department of Medicine, University Hospital of GenevaDepartment of Medicine, University Hospital of Geneva, University of Geneva, Geneva, Switzerland.

Cem Gabay (C)

Division of Rheumatology, Department of Medicine, University Hospital of GenevaDepartment of Medicine, University Hospital of Geneva, University of Geneva, Geneva, Switzerland.

Hartmut Schmidt (H)

Department of Gastroenterology, Hepatology, Endocrinology and Clinical Infectiology, University Hospital Muenster, Muenster, Germany.

Dirk Foell (D)

Department of Pediatric Rheumatology and Immunology, University Children's Hospital Muenster, Muenster, Germany.

Phil-Robin Tepasse (PR)

Department of Gastroenterology, Hepatology, Endocrinology and Clinical Infectiology, University Hospital Muenster, Muenster, Germany.

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