About: Contribution of the Purinergic Receptor P2X7 to Development of Lung Immunopathology during Influenza Virus Infection

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About: Contribution of the Purinergic Receptor P2X7 to Development of Lung Immunopathology during Influenza Virus Infection Goto Sponge NotDistinct Permalink

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Contribution of the Purinergic Receptor P2X7 to Development of Lung Immunopathology during Influenza Virus Infection
Creator	García-Sastre, Adolfo Biron, Christine Lim, Jean Leyva-Grado, Victor Schotsaert, Michael Ermler, Megan Gillespie, Virginia Gonzalez, Ma
Source	PMC
abstract	An exacerbated immune response is one of the main causes of influenza-induced lung damage during infection. The molecular mechanisms regulating the fate of the initial immune response to infection, either as a protective response or as detrimental immunopathology, are not well understood. The purinergic receptor P2X7 is an ionotropic nucleotide-gated ion channel receptor expressed on immune cells that has been implicated in induction and maintenance of excessive inflammation. Here, we analyze the role of this receptor in a mouse model of influenza virus infection using a receptor knockout (KO) mouse strain. Our results demonstrate that the absence of the P2X7 receptor results in a better outcome to influenza virus infection characterized by reduced weight loss and increased survival upon experimental influenza challenge compared to wild-type mice. This effect was not virus strain specific. Overall lung pathology and apoptosis were reduced in virus-infected KO mice. Production of proinflammatory cytokines and chemokines such as interleukin-10 (IL-10), gamma interferon (IFN-γ), and CC chemokine ligand 2 (CCL2) was also reduced in the lungs of the infected KO mice. Infiltration of neutrophils and depletion of CD11b(+) macrophages, characteristic of severe influenza virus infection in mice, were lower in the KO animals. Together, these results demonstrate that activation of the P2X7 receptor is involved in the exacerbated immune response observed during influenza virus infection.
has issue date	2017-03-28(xsd:dateTime)
bibo:doi	10.1128/mbio.00229-17
bibo:pmid	28351919
has license	cc-by
sha1sum (hex)	028382edbe67a35f1e099fa0607fa9a4922a45d1
schema:url	https://doi.org/10.1128/mbio.00229-17
resource representing a document's title	Contribution of the Purinergic Receptor P2X7 to Development of Lung Immunopathology during Influenza Virus Infection
has PubMed Central identifier	PMC5371412
has PubMed identifier	28351919
schema:publication	mBio
resource representing a document's body	covid:028382edbe67a35f1e099fa0607fa9a4922a45d1#body_text
is schema:about of	named entity 'LUNG' named entity 'observed' named entity 'severe' named entity 'infected' named entity 'wild-type' named entity 'The' named entity 'clearance' named entity 'P2X7' named entity 'Receptor' named entity 'VIRUS INFECTION' named entity 'FATE' named entity 'ANTIVIRAL' named entity 'INTERLEUKIN-10 ' named entity 'ABSENCE OF' named entity 'ACTIVATION' named entity 'REDUCED WEIGHT' named entity 'INFLUENZA VIRUS' named entity 'IMMUNOPATHOLOGY' named entity 'SEVERE' named entity 'INFECTED' named entity 'IMMUNE CELLS' named entity 'RESPONSE TO' named entity 'NUCLEOTIDE' covid:arg/028382edbe67a35f1e099fa0607fa9a4922a45d1 named entity '10%' named entity 'UNDERSTOOD' named entity 'SURVIVAL' named entity 'CD11B' named entity '90%' named entity 'INFILTRATION' named entity 'RESPONSE' named entity 'MOUSE MODEL' named entity 'PURINERGIC RECEPTOR' named entity 'CAUSES' named entity 'MAINTENANCE' named entity 'INCREASED' named entity 'PRODUCTION' named entity 'PURINERGIC RECEPTOR' named entity 'P2X7' named entity 'DEVELOPMENT' named entity 'EXACERBATED' named entity 'MAIN' named entity 'OUR' named entity 'CHEMOKINES' named entity 'NEUTROPHILS' named entity 'MICE' named entity 'CONTRIBUTION' named entity 'INVOLVED' named entity 'NOT WELL' named entity 'USING' named entity 'USED' named entity 'IMMUNE RESPONSE' named entity 'INFECTION' named entity 'PARTICULAR' named entity 'INFLUENZA VIRUS' named entity 'CC CHEMOKINE' named entity 'COMPARED' named entity 'DEVELOPMENT' named entity 'LEAD' named entity 'INITIAL' named entity 'LUNG' named entity 'HERE' named entity 'EXCESSIVE' named entity 'SPECIFIC' named entity 'GATED ION CHANNEL' named entity 'PROINFLAMMATORY CYTOKINES' named entity 'OUTCOME' named entity 'OVERALL' named entity 'EITHER' named entity 'INFLAMMATION' named entity 'IMMUNOPATHOLOGY' named entity 'REGULATING' named entity 'REQUIRED' named entity 'CHARACTERISTIC'

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