SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection

Abstract New influenza A viruses that emerge frequently elicit composite inflammatory responses to both infection and structural damage of alveolar-capillary barrier cells that hinders regeneration of respiratory function. The host factors that relinquish restoration of lung health to enduring lung...

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Autores principales:	Kristin K. Fino, Linlin Yang, Patricia Silveyra, Sanmei Hu, Todd M. Umstead, Susan DiAngelo, E. Scott Halstead, Timothy K. Cooper, Thomas Abraham, Yoshinori Takahashi, Zhixiang Zhou, Hong Gang Wang, Zissis C. Chroneos
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9f2db467b2f24fcdb539803d205c307c
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spelling	oai:doaj.org-article:9f2db467b2f24fcdb539803d205c307c2021-12-02T12:31:51ZSH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection10.1038/s41598-017-07724-52045-2322https://doaj.org/article/9f2db467b2f24fcdb539803d205c307c2017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07724-5https://doaj.org/toc/2045-2322Abstract New influenza A viruses that emerge frequently elicit composite inflammatory responses to both infection and structural damage of alveolar-capillary barrier cells that hinders regeneration of respiratory function. The host factors that relinquish restoration of lung health to enduring lung injury are insufficiently understood. Here, we investigated the role of endophilin B2 (B2) in susceptibility to severe influenza infection. WT and B2-deficient mice were infected with H1N1 PR8 by intranasal administration and course of influenza pneumonia, inflammatory, and tissue responses were monitored over time. Disruption of B2 enhanced recovery from severe influenza infection as indicated by swift body weight recovery and significantly better survival of endophilin B2-deficient mice compared to WT mice. Compared to WT mice, the B2-deficient lungs exhibited induction of genes that express surfactant proteins, ABCA3, GM-CSF, podoplanin, and caveolin mRNA after 7 days, temporal induction of CCAAT/enhancer binding protein CEBPα, β, and δ mRNAs 3–14 days after infection, and differences in alveolar extracellular matrix integrity and respiratory mechanics. Flow cytometry and gene expression studies demonstrated robust recovery of alveolar macrophages and recruitment of CD4+ lymphocytes in B2-deficient lungs. Targeting of endophilin B2 alleviates adverse effects of IAV infection on respiratory and immune cells enabling restoration of alveolar homeostasis.Kristin K. FinoLinlin YangPatricia SilveyraSanmei HuTodd M. UmsteadSusan DiAngeloE. Scott HalsteadTimothy K. CooperThomas AbrahamYoshinori TakahashiZhixiang ZhouHong Gang WangZissis C. ChroneosNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-17 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Kristin K. Fino Linlin Yang Patricia Silveyra Sanmei Hu Todd M. Umstead Susan DiAngelo E. Scott Halstead Timothy K. Cooper Thomas Abraham Yoshinori Takahashi Zhixiang Zhou Hong Gang Wang Zissis C. Chroneos SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection
description	Abstract New influenza A viruses that emerge frequently elicit composite inflammatory responses to both infection and structural damage of alveolar-capillary barrier cells that hinders regeneration of respiratory function. The host factors that relinquish restoration of lung health to enduring lung injury are insufficiently understood. Here, we investigated the role of endophilin B2 (B2) in susceptibility to severe influenza infection. WT and B2-deficient mice were infected with H1N1 PR8 by intranasal administration and course of influenza pneumonia, inflammatory, and tissue responses were monitored over time. Disruption of B2 enhanced recovery from severe influenza infection as indicated by swift body weight recovery and significantly better survival of endophilin B2-deficient mice compared to WT mice. Compared to WT mice, the B2-deficient lungs exhibited induction of genes that express surfactant proteins, ABCA3, GM-CSF, podoplanin, and caveolin mRNA after 7 days, temporal induction of CCAAT/enhancer binding protein CEBPα, β, and δ mRNAs 3–14 days after infection, and differences in alveolar extracellular matrix integrity and respiratory mechanics. Flow cytometry and gene expression studies demonstrated robust recovery of alveolar macrophages and recruitment of CD4+ lymphocytes in B2-deficient lungs. Targeting of endophilin B2 alleviates adverse effects of IAV infection on respiratory and immune cells enabling restoration of alveolar homeostasis.
format	article
author	Kristin K. Fino Linlin Yang Patricia Silveyra Sanmei Hu Todd M. Umstead Susan DiAngelo E. Scott Halstead Timothy K. Cooper Thomas Abraham Yoshinori Takahashi Zhixiang Zhou Hong Gang Wang Zissis C. Chroneos
author_facet	Kristin K. Fino Linlin Yang Patricia Silveyra Sanmei Hu Todd M. Umstead Susan DiAngelo E. Scott Halstead Timothy K. Cooper Thomas Abraham Yoshinori Takahashi Zhixiang Zhou Hong Gang Wang Zissis C. Chroneos
author_sort	Kristin K. Fino
title	SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection
title_short	SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection
title_full	SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection
title_fullStr	SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection
title_full_unstemmed	SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection
title_sort	sh3glb2/endophilin b2 regulates lung homeostasis and recovery from severe influenza a virus infection
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/9f2db467b2f24fcdb539803d205c307c
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SH3GLB2/endophilin B2 regulates lung homeostasis and recovery from severe influenza A virus infection

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