The annexin A1/FPR2 signaling axis expands alveolar macrophages, limits viral replication, and attenuates pathogenesis in the murine influenza A virus infection model.
Animals
Annexin A1
/ physiology
Disease Models, Animal
Granulocyte-Macrophage Colony-Stimulating Factor
/ physiology
Influenza A virus
/ pathogenicity
Macrophages, Alveolar
/ immunology
Male
Mice
Mice, Inbred C57BL
Orthomyxoviridae Infections
/ prevention & control
Receptors, Formyl Peptide
/ physiology
Signal Transduction
/ physiology
Virus Replication
innate immune system
mucosal immunity
pattern recognition receptors
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
11 2019
11 2019
Historique:
pubmed:
10
8
2019
medline:
29
5
2020
entrez:
10
8
2019
Statut:
ppublish
Résumé
Pattern recognition receptors (PRRs) are key elements in the innate immune response. Formyl peptide receptor (FPR) 2 is a PRR that, in addition to proinflammatory, pathogen-derived compounds, also recognizes the anti-inflammatory endogenous ligand annexin A1 (AnxA1). Because the contribution of this signaling axis in viral infections is undefined, we investigated AnxA1-mediated FPR2 activation on influenza A virus (IAV) infection in the murine model. AnxA1-treated mice displayed significantly attenuated pathology upon a subsequent IAV infection with significantly improved survival, impaired viral replication in the respiratory tract, and less severe lung damage. The AnxA1-mediated protection against IAV infection was not caused by priming of the type I IFN response but was associated with an increase in the number of alveolar macrophages (AMs) and enhanced pulmonary expression of the AM-regulating cytokine granulocyte-M-CSF (GM-CSF). Both AnxA1-mediated increase in AM levels and GM-CSF production were abrogated when mouse (m)FPR2 signaling was antagonized but remained up-regulated in mice genetically deleted for mFPR1, an mFPR2 isoform also serving as AnxA1 receptor. Our results indicate a novel protective function of the AnxA1-FPR2 signaling axis in IAV pathology
Identifiants
pubmed: 31398292
doi: 10.1096/fj.201901265R
pmc: PMC6902725
doi:
Substances chimiques
Annexin A1
0
Receptors, Formyl Peptide
0
annexin A1, mouse
0
formyl peptide receptor 2, mouse
0
Granulocyte-Macrophage Colony-Stimulating Factor
83869-56-1
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
12188-12199Références
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