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

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 administere

SUBMITTER: Hassett P 

PROVIDER: S-EPMC7095197 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature