Pulmonary SARS-CoV-2 infection leads to para-infectious immune activation in the brain.
SARS-CoV-2
immunology
microglia
neurology
virology
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2024
2024
Historique:
received:
29
05
2024
accepted:
04
09
2024
medline:
30
10
2024
pubmed:
30
10
2024
entrez:
30
10
2024
Statut:
epublish
Résumé
Neurological complications, including encephalopathy and stroke, occur in a significant proportion of COVID-19 cases but viral protein is seldom detected in the brain parenchyma. To model this situation, we developed a novel low-inoculum K18-hACE2 mouse model of SARS-CoV-2 infection during which active viral replication was consistently seen in mouse lungs but not in the brain. We found that several mediators previously associated with encephalopathy in clinical samples were upregulated in the lung, including CCL2, and IL-6. In addition, several inflammatory mediations, including CCL4, IFNγ, IL-17A, were upregulated in the brain, associated with microglial reactivity. Parallel
Identifiants
pubmed: 39474424
doi: 10.3389/fimmu.2024.1440324
pmc: PMC11519853
doi:
Substances chimiques
Angiotensin-Converting Enzyme 2
EC 3.4.17.23
Cytokines
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1440324Informations de copyright
Copyright © 2024 Dunai, Hetherington, Boardman, Clark, Sharma, Subramaniam, Tharmaratnam, Needham, Williams, Huang, Wood, Collie, Fower, Fox, Ellul, Held, Egbe, Griffiths, Solomon, Breen, Kipar, Cavanagh, Irani, Vincent, Stewart, Taams, Menon and Michael.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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