Rare SOX2+ Airway Progenitor Cells Generate KRT5+ Cells that Repopulate Damaged Alveolar Parenchyma following Influenza Virus Infection.
Abstract
Recent studies have implicated keratin 5 (KRT5)+ cells in repopulation of damaged
lung tissue following severe H1N1 influenza virus infection. However, the origins
of the cells repopulating the injured alveolar region remain controversial. We sought
to determine the cellular dynamics of lung repair following influenza infection and
define whether nascent KRT5+ cells repopulating alveolar epithelium were derived from
pre-existing alveolar or airway progenitor cells. We found that the wound-healing
response begins with proliferation of SOX2+ SCGB1A1- KRT5- progenitor cells in airways.
These cells generate nascent KRT5+ cells as an early response to airway injury and
yield progeny that colonize damaged alveolar parenchyma. Moreover, we show that local
alveolar progenitors do not contribute to nascent KRT5+ cells after injury. Repopulation
of injured airway and alveolar regions leads to proximalization of distal airways
by pseudostratified epithelium and of alveoli by airway-derived epithelial cells that
lack the normal characteristics of mature airway or alveolar epithelium.
Type
Journal articleSubject
Respiratory MucosaStem Cells
Animals
Mice, Transgenic
Mice
Orthomyxoviridae Infections
Cell Differentiation
Cell Lineage
Models, Biological
Influenza A Virus, H1N1 Subtype
Keratin-5
SOXB1 Transcription Factors
Biomarkers
Cell Self Renewal
Alveolar Epithelial Cells
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https://hdl.handle.net/10161/22235Published Version (Please cite this version)
10.1016/j.stemcr.2016.09.010Publication Info
Ray, Samriddha; Chiba, Norika; Yao, Changfu; Guan, Xiangrong; McConnell, Alicia M;
Brockway, Brian; ... Stripp, Barry R (2016). Rare SOX2+ Airway Progenitor Cells Generate KRT5+ Cells that Repopulate Damaged Alveolar
Parenchyma following Influenza Virus Infection. Stem cell reports, 7(5). pp. 817-825. 10.1016/j.stemcr.2016.09.010. Retrieved from https://hdl.handle.net/10161/22235.This is constructed from limited available data and may be imprecise. To cite this
article, please review & use the official citation provided by the journal.
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Show full item recordScholars@Duke
Loretta Georgina Que
Professor of Medicine
My research interests focus on studying the role of nitric oxide and related enzymes
in the pathogenesis of lung disease, specifically that caused by nitrosative/oxidative
stress. Proposed studies are performed in cell culture and applied to animal models
of disease, then examined in human disease where relevant. It is our hope that by
better understanding the role of NO and reactive nitrogen species in mediating inflammation,
and regulating cell signaling, that we will not only help to unr

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