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Am J Respir Cell Mol Biol ; 66(3): 312-322, 2022 03.
Article in English | MEDLINE | ID: mdl-34861136

ABSTRACT

Respiratory syncytial virus (RSV)-induced immunopathogenesis and disease severity in neonatal mice and human infants have been related to elevated pulmonary IL-33. Thus, targeting IL-33 has been suggested as a potential therapy for respiratory viral infections. Yet, the regulatory mechanisms on IL-33 during early life remain unclear. Here, using a neonatal mouse model of RSV, we demonstrate that IL-1ß positively regulates but is not required for RSV-induced expression of pulmonary IL-33 in neonatal mice early after the initial infection. Exogenous IL-1ß upregulates RSV-induced IL-33 expression by promoting the proliferation of IL-33+ lung epithelial stem/progenitor cells. These cells are exclusively detected in RSV-infected neonatal rather than adult mice, partially explaining the IL-1ß-independent IL-33 expression in RSV-infected adult mice. Furthermore, IL-1ß aggravates IL-33-mediated T-helper cell type 2-biased immunopathogenesis upon reinfection. Collectively, our study demonstrates that IL-1ß exacerbates IL-33-mediated RSV immunopathogenesis by promoting the proliferation of IL-33+ epithelial stem/progenitor cells in early life.


Subject(s)
Interleukin-1beta/pharmacology , Respiratory Syncytial Virus Infections , Respiratory Syncytial Virus, Human , Animals , Humans , Interleukin-33 , Lung/pathology , Mice , Mice, Inbred BALB C , Respiratory Syncytial Virus Infections/pathology , Stem Cells/pathology
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