SARS-CoV-2 infection damages airway motile cilia and impairs mucociliary clearance
Robinot, R.; Hubert, M.; Dias de Melo, G.; Lazarini, F.; Bruel, T.; Smith, N.; Levallois, S.; Larrous, F.; Fernandes, J.; Gellenoncourt, S.; Rigaud, S.; Gorgette, O.; Thouvenot, C.; Trebeau, C.; Dumenil, G.; Mallet, A.; Gobaa, S.; Etournay, R.; Lledo, P.-M.; Lecuit, M.; Bourhy, H.; Duffy, D.; Michel, V.; Schwartz, O.; Chakrabarti, L. A.
Show abstract
Understanding how SARS-CoV-2 spreads within the respiratory tract is important to define the parameters controlling the severity of COVID-19. We examined the functional and structural consequences of SARS-CoV-2 infection in a reconstituted human bronchial epithelium model. SARS-CoV-2 replication caused a transient decrease in epithelial barrier function and disruption of tight junctions, though viral particle crossing remained limited. Rather, SARS-CoV-2 replication led to a rapid loss of the ciliary layer, characterized at the ultrastructural level by axoneme loss and misorientation of remaining basal bodies. The motile cilia function was compromised, as measured in a mucociliary clearance assay. Epithelial defense mechanisms, including basal cell mobilization and interferon-lambda induction, ramped up only after the initiation of cilia damage. Analysis of SARS-CoV-2 infection in Syrian hamsters further demonstrated the loss of motile cilia in vivo. This study identifies cilia damage as a pathogenic mechanism that could facilitate SARS-CoV-2 spread to the deeper lung parenchyma.
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