Pulmonary mesenchymal stem cells are engaged in distinct steps of host response to respiratory syncytial virus infection

Lung-resident (LR) mesenchymal stem and stromal cells (MSCs) are key elements of the alveolar niche and fundamental regulators of homeostasis and regeneration. We interrogated their function during virus-induced lung injury using the highly prevalent respiratory syncytial virus (RSV) which causes se...

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Bibliographic Details
Published in:PLoS pathogens 2021-07, Vol.17 (7), p.e1009789-e1009789
Main Authors: Brügger, Melanie, Démoulins, Thomas, Barut, G. Tuba, Zumkehr, Beatrice, Oliveira Esteves, Blandina I, Mehinagic, Kemal, Haas, Quentin, Schögler, Aline, Rameix-Welti, Marie-Anne, Eléouët, Jean-François, Moehrlen, Ueli, Marti, Thomas M, Schmid, Ralph A, Summerfield, Artur, Posthaus, Horst, Ruggli, Nicolas, Hall, Sean R. R, Alves, Marco P
Format: Article
Language:English
Subjects:
Alveoli
Angiogenesis
Biology and Life Sciences
Connective tissue cells
Development and progression
Health aspects
Homeostasis
Host-virus relationships
Immune response
Infections
Inflammation
Life Sciences
Lungs
Lymphocytes
Lymphocytes T
Medicine and Health Sciences
Mesenchymal stem cells
Mesenchyme
Microscopy
Pediatrics
Phenotypes
Physiological aspects
Proteins
Regeneration
Respiratory syncytial virus
Respiratory syncytial virus infection
Stem cells
Stromal cells
Transcription
Viruses
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Summary:Lung-resident (LR) mesenchymal stem and stromal cells (MSCs) are key elements of the alveolar niche and fundamental regulators of homeostasis and regeneration. We interrogated their function during virus-induced lung injury using the highly prevalent respiratory syncytial virus (RSV) which causes severe outcomes in infants. We applied complementary approaches with primary pediatric LR-MSCs and a state-of-the-art model of human RSV infection in lamb. Remarkably, RSV-infection of pediatric LR-MSCs led to a robust activation, characterized by a strong antiviral and pro-inflammatory phenotype combined with mediators related to T cell function. In line with this, following in vivo infection, RSV invades and activates LR-MSCs, resulting in the expansion of the pulmonary MSC pool. Moreover, the global transcriptional response of LR-MSCs appears to follow RSV disease, switching from an early antiviral signature to repair mechanisms including differentiation, tissue remodeling, and angiogenesis. These findings demonstrate the involvement of LR-MSCs during virus-mediated acute lung injury and may have therapeutic implications.
ISSN:1553-7374
1553-7366
1553-7374
DOI:10.1371/journal.ppat.1009789