SARS-CoV-2, which induces COVID-19, causes kawasaki-like disease in children: role of pro-inflammatory and anti-inflammatory cytokines.


Journal

Journal of biological regulators and homeostatic agents
ISSN: 0393-974X
Titre abrégé: J Biol Regul Homeost Agents
Pays: Italy
ID NLM: 8809253

Informations de publication

Date de publication:
Historique:
entrez: 2 6 2020
pubmed: 2 6 2020
medline: 24 9 2020
Statut: ppublish

Résumé

Acute severe respiratory syndrome coronavirus-2 (SARS-CoV-2) caused a global pandemic coronavirus disease 2019 (COVID-19). In humans, SARS-CoV-2 infection leads to acute respiratory distress syndrome which presents edema, hemorrhage, intra-alveolar fibrin deposition, and vascular changes characterized by thrombus formation, micro-angiopathy and thrombosis. These clinical signs are mediated by pro-inflammatory cytokines. In recent studies it has been noted that COVID-19 pandemic can affect patients of all ages, including children (even if less severely) who were initially thought to be immune. Kawasaki disease is an autoimmune acute febrile inflammatory condition, which primarily affects young children. The disease can present immunodeficiency with the inability of the immune system to fight inflammatory pathogens and leads to fever, rash, alterations of the mucous membranes, conjunctiva infection, pharyngeal erythema, adenopathy, and inflammation. In the COVID-19 period, virus infection aggravates the condition of Kawasaki disease, but it has also been noted that children affected by SARS-V-2 may develop a disease similar to Kawasaki's illness. However, it is uncertain whether the virus alone can give Kawasaki disease-like forms. As in COVID-19, Kawasaki disease and its similar forms are mediated by pro-inflammatory cytokines produced by innate immunity cells such as macrophages and mast cells (MCs). In light of the above, it is therefore pertinent to think that by blocking pro-inflammatory cytokines with new anti-inflammatory cytokines, such as IL-37 and IL-38, it is possible to alleviate the symptoms of the disease and have a new available therapeutic tool. However, since Kawasaki and Kawasaki-like diseases present immunodeficiency, treatment with anti-inflammatory/immunosuppressant molecules must be applied very carefully.

Identifiants

pubmed: 32476380
doi: 10.23812/EDITORIAL-RONCONI-E-59
pii: 59
doi:

Substances chimiques

Cytokines 0
IL-38 protein, human 0
IL37 protein, human 0
Interleukin-1 0
Interleukins 0

Types de publication

Editorial

Langues

eng

Sous-ensembles de citation

IM

Pagination

767-773

Informations de copyright

Copyright 2020 Biolife Sas. www.biolifesas.org.

Auteurs

G Ronconi (G)

Clinica dei Pazienti del Territorio, Fondazione Policlinico Gemelli, Rome, Italy.

G Teté (G)

Specialization School in Oral Surgery, Vita-Salute San Raffaele University, Milan, Italy.

S K Kritas (SK)

Department of Microbiology and Infectious Diseases, School of Veterinary Medicine, Aristotle University of Thessaloniki, Macedonia, Greece.

C E Gallenga (CE)

Department of Biomedical Sciences and Specialist Surgery, Section of Ophthalmology, University of Ferrara, Ferrara, Italy.

Al Caraffa (Al)

School of Pharmacy, University of Camerino, Camerino, Italy.

R Ross (R)

University of Pennsylvania School of Veterinary Medicine, Philadelphia, PA, USA.

P Conti (P)

Postgraduate Medical School, University of Chieti, Chieti, Italy.

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Classifications MeSH