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Acute Respiratory Distress Syndrome (ARDS): Are corticosteroids harmful in lung injury
Author(s) -
Chupin Cecile,
Lavoie Jacynthe,
Privé Anik,
Brochiero Emmanuelle,
Berthiaume Yves
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.865.5
Subject(s) - ards , dexamethasone , medicine , lung , bleomycin , inflammation , apoptosis , respiratory distress , anesthesia , endocrinology , biology , chemotherapy , biochemistry
ARDS is a rapidly evolving lung injury that is linked with permeability oedema and excessive inflammation, leading to a severe oxygenation defect. Albeit there has been significant progress in survival, ARDS mortality remains ~ 40 %. Glucocorticoids therapy has been proposed to decrease the inflammatory response, but its usage remains controversial. The objective of this study was to evaluate the impact of dexamethasone treatment (dex; 0.5 mg/kg/d) on the in vivo evolution of bleomycin‐induced (bleo; 4 U/kg) lung injury in NMRI mouse. Treatment with dex did not decrease the mortality, the weight loss, the wet/dry ratio, the severity of epithelial injuries and the inflammatory infiltrating of neutrophils induced by bleo. To better evaluate the lack of response to dex, the impact of dex on the repair process of primary epithelial cells was studied. Our results show that dex inhibits the closure of mechanical wound. This effect of dex is not related to a default of proliferation, or an activation of apoptosis. This inhibitory effect of dex on wound closure is associated with an increase in cell adhesion suggesting that its effect could be related a modulation of the cytoskeleton. Our results indicate that dex does not decrease the severity of lung injury model and might slow its recovery by preventing proper repair of the alveolar epithelium. Supported by RSR‐FRSQ, FCFK, IRSC.