About: An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens

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An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens
Creator	Schultz-Cherry, Stacey Sharma, Shalini Vogel, Peter Duan, Susu Johnson, Michael Bosio, Catharine Guy, Cliff Jolly, Lisa Neale, Geoff Sheppard, Dean Meliopoulos, Victoria Thomas, Paul Hurwitz, Julia Karlsson, Erik Jenkins, R Jones, Bart Murray, Peter Rosch, Jason Surman, Sherri Van De Velde, Van De Velde, Lee-Ann
Source	Medline; PMC
abstract	The healthy lung maintains a steady state of immune readiness to rapidly respond to injury from invaders. Integrins are important for setting the parameters of this resting state, particularly the epithelial-restricted αVβ6 integrin, which is upregulated during injury. Once expressed, αVβ6 moderates acute lung injury (ALI) through as yet undefined molecular mechanisms. We show that the upregulation of β6 during influenza infection is involved in disease pathogenesis. β6-deficient mice (β6 KO) have increased survival during influenza infection likely due to the limited viral spread into the alveolar spaces leading to reduced ALI. Although the β6 KO have morphologically normal lungs, they harbor constitutively activated lung CD11b(+) alveolar macrophages (AM) and elevated type I IFN signaling activity, which we traced to the loss of β6-activated transforming growth factor-β (TGF-β). Administration of exogenous TGF-β to β6 KO mice leads to reduced numbers of CD11b(+) AMs, decreased type I IFN signaling activity and loss of the protective phenotype during influenza infection. Protection extended to other respiratory pathogens such as Sendai virus and bacterial pneumonia. Our studies demonstrate that the loss of one epithelial protein, αVβ6 integrin, can alter the lung microenvironment during both homeostasis and respiratory infection leading to reduced lung injury and improved survival.
has issue date	2016-08-09(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1005804
bibo:pmid	27505057
has license	cc0
sha1sum (hex)	2c7f8c9a78ec06b29ea61f2dd02730d2c3af1cfb
schema:url	https://doi.org/10.1371/journal.ppat.1005804
resource representing a document's title	An Epithelial Integrin Regulates the Amplitude of Protective Lung Interferon Responses against Multiple Respiratory Pathogens
has PubMed Central identifier	PMC4978498
has PubMed identifier	27505057
schema:publication	PLoS Pathog
resource representing a document's body	covid:2c7f8c9a78ec06b29ea61f2dd02730d2c3af1cfb#body_text
is schema:about of	named entity 'morphologically' named entity 'involved' named entity 'macrophages' named entity 'improved' named entity 'signaling' named entity 'mice' named entity 'TGF-β' named entity 'Protection' named entity 'integrin' named entity 'Respiratory' named entity 'Integrin' covid:arg/2c7f8c9a78ec06b29ea61f2dd02730d2c3af1cfb named entity 'survival' named entity 'microenvironment' named entity 'constitutively' named entity 'Once' named entity 'Integrins' named entity 'PLOS Pathogens' named entity 'normal' named entity 'lung' named entity 'traced' named entity 'Interferon' named entity 'integrin' named entity 'protein' named entity 'alveolar macrophages' named entity 'acute lung injury' named entity 'phenotype' named entity 'homeostasis' named entity 'molecular mechanisms' named entity 'ALI' named entity 'epithelial' named entity 'type I IFN' named entity 'lung' named entity 'microenvironment' named entity 'influenza infection' named entity 'Integrins' named entity 'steady state' named entity 'pathogenesis' named entity 'Lung' named entity 'Epithelial' named entity 'PBS' named entity 'PCR' named entity 'post-translational processing' named entity '0.01' named entity 'influenza infection' named entity 'KO mice' named entity 'fibronectin' named entity 'KO mice' named entity 'type I IFN' named entity '0.01' named entity 'CD45' named entity 'chemokines' named entity 'formalin' named entity 'CFU' named entity 'upregulation' named entity 'epithelial' named entity 'KO mice' named entity 'ALI' named entity 'viruses' named entity 'RNA' named entity 'homogenates'

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