About: GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization

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About: GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization
Creator	Silveyra, Patricia Chroneos, Zissis Umstead, Todd Kawasawa, Yuka Davies, Michael Guo, Weichao Halstead, E Hewage, Eranda Howyrlak, Judie Hu, Sanmei Yang, Linlin
topic	covid:7d2d4ad7dedaa66a5e699e2986e30f9db2df4b8e#this
Source	PMC
abstract	BACKGROUND: Influenza A viruses cause life-threatening pneumonia and lung injury in the lower respiratory tract. Application of high GM-CSF levels prior to infection has been shown to reduce morbidity and mortality from pathogenic influenza infection in mice, but the mechanisms of protection and treatment efficacy have not been established. METHODS: Mice were infected intranasally with influenza A virus (PR8 strain). Supra-physiologic levels of GM-CSF were induced in the airways using the double transgenic GM-CSF (DTGM) or littermate control mice starting on 3 days post-infection (dpi). Assessment of respiratory mechanical parameters was performed using the flexiVent rodent ventilator. RNA sequence analysis was performed on FACS-sorted airway macrophage subsets at 8 dpi. RESULTS: Supra-physiologic levels of GM-CSF conferred a survival benefit, arrested the deterioration of lung mechanics, and reduced the abundance of protein exudates in bronchoalveolar (BAL) fluid to near baseline levels. Transcriptome analysis, and subsequent validation ELISA assays, revealed that excess GM-CSF re-directs macrophages from an “M1-like” to a more “M2-like” activation state as revealed by alterations in the ratios of CXCL9 and CCL17 in BAL fluid, respectively. Ingenuity pathway analysis predicted that GM-CSF surplus during IAV infection elicits expression of anti-inflammatory mediators and moderates M1 macrophage pro-inflammatory signaling by Type II interferon (IFN-γ). CONCLUSIONS: Our data indicate that application of high levels of GM-CSF in the lung after influenza A virus infection alters pathogenic “M1-like” macrophage inflammation. These results indicate a possible therapeutic strategy for respiratory virus-associated pneumonia and acute lung injury. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12931-017-0708-5) contains supplementary material, which is available to authorized users.
has issue date	2018-01-05(xsd:dateTime)
bibo:doi	10.1186/s12931-017-0708-5
bibo:pmid	29304863
has license	cc-by
sha1sum (hex)	7d2d4ad7dedaa66a5e699e2986e30f9db2df4b8e
schema:url	https://doi.org/10.1186/s12931-017-0708-5
resource representing a document's title	GM-CSF overexpression after influenza a virus infection prevents mortality and moderates M1-like airway monocyte/macrophage polarization
has PubMed Central identifier	PMC5756339
has PubMed identifier	29304863
schema:publication	Respir Res
resource representing a document's body	covid:7d2d4ad7dedaa66a5e699e2986e30f9db2df4b8e#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/7d2d4ad7dedaa66a5e699e2986e30f9db2df4b8e
is schema:about of	named entity 'morbidity' named entity 'pneumonia' named entity 'influenza' named entity 'LIFE' named entity 'TO REDUCE' named entity 'BUT' named entity 'TREATMENT EFFICACY' named entity 'ESTABLISHED' named entity 'MICE' named entity 'virus' named entity 'influenza infection' named entity 'lower respiratory tract' named entity 'genetic background' named entity 'infection' named entity 'Arg1' named entity 'IPA' named entity 'wild-type' named entity 'interferon regulatory factor 3' named entity 'GM-CSF' named entity 'transcriptome' named entity 'CCL17' named entity 'alveolar macrophages' named entity 'nuclear factor kappa-B' named entity 'Luminex' named entity 'alveolar macrophage' named entity 'differential gene expression' named entity 'xylazine' named entity 'ventilation/perfusion mismatch' named entity 'ethanol' named entity 'p-value' named entity 'tumor suppressor protein' named entity 'Becton Dickinson' named entity 'monomer' named entity 'cytokine' named entity 'specific pathogen free' named entity 'M-CSF' named entity 'over-expression' named entity 'GM-CSF' named entity 'body weight' named entity 'GM-CSF' named entity 'infection' named entity 'infection' named entity 'Alveolar macrophages' named entity 'homogenized' named entity 'IPA' named entity 'infection' named entity 'p53' named entity 'therapeutic benefit' named entity 'GM-CSF' named entity 'transcriptome' named entity 'p-value' named entity 'IAV' named entity 'DIP' named entity 'doxycycline' named entity 'infection' named entity 'centrifugation' named entity 'infection' named entity 'GM-CSF' named entity 'IAV' named entity 'MMP12' named entity 'infection' named entity 'Illumina' named entity 'inflammation' named entity 'positive end expiratory pressure' named entity 'immune response' named entity 'GM-CSF' named entity 'RNA' named entity 'doxycycline' named entity 'Alveolar macrophages'

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