Autor: |
Vu, Luan D., Phan, Anh T. Q., Hijano, Diego R., Siefker, David T., Tillman, Heather, Cormier, Stephania A. |
Předmět: |
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Zdroj: |
American Journal of Respiratory Cell & Molecular Biology; Mar2022, Vol. 66 Issue 3, p312-322, 11p |
Abstrakt: |
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-1β positively regulates but is not required for RSV-induced expression of pulmonary IL-33 in neonatal mice early after the initial infection. Exogenous IL-1β upregulates RSV-induced IL-33 expression by promoting the proliferation of IL-331 lung epithelial stem/progenitor cells. These cells are exclusively detected in RSV-infected neonatal rather than adult mice, partially explaining the IL-1β–independent IL-33 expression in RSV-infected adult mice. Furthermore, IL-1β aggravates IL-33–mediated T-helper cell type 2–biased immunopathogenesis upon reinfection. Collectively, our study demonstrates that IL-1β exacerbates IL-33–mediated RSV immunopathogenesis by promoting the proliferation of IL-33+ epithelial stem/progenitor cells in early life. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
Externí odkaz: |
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