Role of CCR3 in respiratory syncytial virus infection of airway epithelial cells.

Fiche publication

Date publication

décembre 2021

Journal

iScience

Auteurs

Membres identifiés du Cancéropôle Est :
Dr DORMOY Valerian

Tous les auteurs :
Wellemans V, Benhassou HA, Fuselier E, Bellesort F, Dury S, Lebargy F, Dormoy V, Fichel C, Naour RL, Gounni AS, Lamkhioued B

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/34917892

Résumé

Respiratory syncytial virus () infection is the principal cause of severe lower respiratory tract disease and accounts for a significant risk for developing asthma later in life. Clinical studies have shown an increase in airway responsiveness and a concomitant Th response in the lungs of RSV-infected patients. These indications suggest that RSV may modulate aspects of the immune response to promote virus replication. Here, we show that CCR3 facilitates RSV infection of airway epithelial cells, an effect that was inhibited by eotaxin-1/CCL11 or upon CCR3 gene silencing. Mechanistically, cellular entry of RSV is mediated by binding of the viral G protein to CCR3 and selective chemotaxis of Th cells and eosinophils. In vivo, mice lacking CCR3 display a significant reduction in RSV infection, airway inflammation, and mucus production. Overall, RSV G protein-CCR3 interaction may participate in pulmonary infection and inflammation by enhancing eosinophils' recruitment and less potent antiviral Th cells.