About: Fas-deficient mice have impaired alveolar neutrophil recruitment and decreased expression of anti-KC autoantibody:KC complexes in a model of acute lung injury

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About: Fas-deficient mice have impaired alveolar neutrophil recruitment and decreased expression of anti-KC autoantibody:KC complexes in a model of acute lung injury Goto Sponge NotDistinct Permalink

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	Fas-deficient mice have impaired alveolar neutrophil recruitment and decreased expression of anti-KC autoantibody:KC complexes in a model of acute lung injury
Creator	Matute-Bello, Gustavo Altemeier, William Farnand, Alex Florence, Jon Gil, Sucheol Gill, Sean Krupa, Agnieszka Kurdowska, Anna
Source	PMC
abstract	BACKGROUND: Exposure to mechanical ventilation enhances lung injury in response to various stimuli, such as bacterial endotoxin (LPS). The Fas/FasL system is a receptor ligand system that has dual pro-apoptotic and pro-inflammatory functions and has been implicated in the pathogenesis of lung injury. In this study we test the hypothesis that a functioning Fas/FasL system is required for the development of lung injury in mechanically ventilated mice. METHODS: C57BL/6 (B6) and Fas-deficient lpr mice were exposed to either intra-tracheal PBS followed by spontaneous breathing or intra-tracheal LPS followed by four hours mechanical ventilation with tidal volumes of 10 mL/kg, respiratory rate of 150 breaths per minute, inspired oxygen 0.21 and positive end expiratory pressure (PEEP) of 3 cm of water. RESULTS: Compared with the B6 mice, the lpr mice showed attenuation of the neutrophilic response as measured by decreased numbers of BAL neutrophils and lung myeloperoxidase activity. Interestingly, the B6 and lpr mice had similar concentrations of pro-inflammatory cytokines, including CXCL1 (KC), and similar measurements of permeability and apoptosis. However, the B6 mice showed greater deposition of anti-KC:KC immune complexes in the lungs, as compared with the lpr mice. CONCLUSIONS: We conclude that a functioning Fas/FasL system is required for full neutrophilic response to LPS in mechanically ventilated mice.
has issue date	2012-10-09(xsd:dateTime)
bibo:doi	10.1186/1465-9921-13-91
bibo:pmid	23043753
has license	cc-by
sha1sum (hex)	c96a668e87f4edf85bcb1fae1b377b8e87fa989a
schema:url	https://doi.org/10.1186/1465-9921-13-91
resource representing a document's title	Fas-deficient mice have impaired alveolar neutrophil recruitment and decreased expression of anti-KC autoantibody:KC complexes in a model of acute lung injury
has PubMed Central identifier	PMC3499442
has PubMed identifier	23043753
schema:publication	Respir Res
resource representing a document's body	covid:c96a668e87f4edf85bcb1fae1b377b8e87fa989a#body_text
is schema:about of	named entity 'functioning' named entity 'RECEPTOR LIGAND' named entity 'TEST' named entity 'STUDY' named entity 'mechanical ventilation' named entity 'Fas/FasL' named entity 'development' named entity 'Background' named entity 'dual' named entity 'receptor ligand' named entity 'LPS' named entity 'mice' named entity 'neutrophil' named entity 'alveolar' named entity 'deficient mice' named entity 'fibrosis' named entity 'fraction of inspired oxygen' named entity 'Acute lung injury' named entity 'chemoattractants' named entity 'mice' named entity 'TUNEL' named entity 'immunoglobulins' named entity 'neutrophil' named entity 'mice' named entity 'cytokine' named entity 'cytokeratin' named entity 'apoptotic' named entity 'neutrophils' named entity 'mice' named entity 'IL8' named entity 'PBS' named entity 'PARP' named entity 'permeability' named entity 'HPO' named entity 'autoantibodies' named entity 'PBS' named entity 'mice' named entity 'Neutrophil' named entity 'trachea' named entity 'Muscle relaxation' named entity 'mechanically ventilated' named entity 'Cell Death' named entity 'lung injury' named entity 'Hoechst 33342' named entity 'lungs' named entity 'mechanical ventilation' named entity 'PMN' named entity 'GraphPad Prism' named entity 'deficient mice' named entity 'CXCL1' named entity 'lungs' named entity 'lung injury' named entity 'homogenates' named entity 'bicinchoninic acid' named entity 'hematoxylin and eosin' named entity 'mice' named entity 'clinical setting' named entity 'TUNEL' named entity 'neutrophils' named entity 'homogenate' named entity 'mice' named entity 'Rockford, IL' named entity 'Fc receptors' named entity '0.21' named entity 'mortality rate' named entity 'autoantibodies' named entity 'VEGF' named entity 'membrane surface' named entity 'mice' named entity 'LPS' named entity 'cytokine' named entity 'receptor' named entity 'intubated' named entity 'chemotaxis'

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