Enhanced susceptibility of pediatric airway epithelium to respiratory syncytial virus infection.
Respiratory Syncytial Virus Infections
/ immunology
Humans
Animals
Mice
STAT3 Transcription Factor
/ metabolism
Respiratory Mucosa
/ virology
Apoptosis
Epithelial Cells
/ immunology
Infant
Disease Susceptibility
Respiratory Syncytial Viruses
/ immunology
Child
Lung
/ virology
Respiratory Syncytial Virus, Human
/ immunology
Journal
The Journal of clinical investigation
ISSN: 1558-8238
Titre abrégé: J Clin Invest
Pays: United States
ID NLM: 7802877
Informations de publication
Date de publication:
01 Nov 2024
01 Nov 2024
Historique:
medline:
1
11
2024
pubmed:
1
11
2024
entrez:
1
11
2024
Statut:
epublish
Résumé
Immature innate and adaptive immunity and vulnerability of narrower airways to obstruction increase the susceptibility of infants to severe respiratory syncytial virus (RSV) disease. In this issue of the JCI, Zhao et al. illustrated greater intrinsic susceptibility of pediatric versus adult airway epithelial cells to RSV-induced cytopathology. Using precision cut lung slices (PCLS) and air-liquid interface (ALI) airway epithelial cell cultures, the authors showed that impaired STAT3 activation in RSV-infected pediatric multiciliated cells increased cell apoptosis and viral shedding, which enhanced the spread of infection. Bolstering STAT3 activation and treatment of neonatal mice with apoptosis inhibitors suppressed virus spread, suggesting that enhancing STAT3 activation may provide therapeutic benefit.
Identifiants
pubmed: 39484717
pii: 185689
doi: 10.1172/JCI185689
doi:
pii:
Substances chimiques
STAT3 Transcription Factor
0
STAT3 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM