About: Overexpression of pulmonary extracellular superoxide dismutase attenuates endotoxin-induced acute lung injury

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About: Overexpression of pulmonary extracellular superoxide dismutase attenuates endotoxin-induced acute lung injury 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	Overexpression of pulmonary extracellular superoxide dismutase attenuates endotoxin-induced acute lung injury
Creator	Sepsis, Endotoxin, Á
Source	PMC
abstract	PURPOSE: Superoxide is produced by activated neutrophils during the inflammatory response to stimuli such as endotoxin, can directly or indirectly injure host cells, and has been implicated in the pathogenesis of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). We wished to determine the potential for pulmonary overexpression of the extracellular isoform of superoxide dismutase (EC-SOD) to reduce the severity of endotoxin-induced lung injury. METHODS: Animals were randomly allocated to undergo intratracheal instillation of (1) surfactant alone (vehicle); (2) adeno-associated virus (AAV) vectors containing a null transgene (AAV-null); and (3) adeno-associated virus vectors containing the EC-SOD transgene (AAV-EC-SOD) and endotoxin was subsequently administered intratracheally. Two additional groups were randomized to receive (1) vehicle or (2) AAV-EC-SOD, and to undergo sham (vehicle) injury. The severity of the lung injury was assessed in all animals 24 h later. RESULTS: Endotoxin produced a severe lung injury compared to sham injury. The AAV vector encoding EC-SOD increased lung EC-SOD concentrations, and enhanced the antioxidant capacity of the lung. EC-SOD overexpression decreased the severity of endotoxin-induced ALI, reducing the decrement in systemic oxygenation and lung compliance, decreasing lung permeability and decreasing histologic injury. EC-SOD attenuated pulmonary inflammation, decreased bronchoalveolar lavage neutrophil counts, and reduced interleukin-6 and CINC-1 concentrations. The AAV vector itself did not contribute to inflammation or to lung injury. CONCLUSIONS: Pulmonary overexpression of EC-SOD protects the lung against endotoxin-induced ALI. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s00134-011-2309-y) contains supplementary material, which is available to authorized users.
has issue date	2011-07-14(xsd:dateTime)
bibo:doi	10.1007/s00134-011-2309-y
bibo:pmid	21755396
has license	no-cc
sha1sum (hex)	47c933debd49e6925f132829d299c71d580a2c18
schema:url	https://doi.org/10.1007/s00134-011-2309-y
resource representing a document's title	Overexpression of pulmonary extracellular superoxide dismutase attenuates endotoxin-induced acute lung injury
has PubMed Central identifier	PMC7095197
has PubMed identifier	21755396
schema:publication	Intensive Care Med
resource representing a document's body	covid:47c933debd49e6925f132829d299c71d580a2c18#body_text
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