Giuseppe
Emeritus
[Source: The Lancet Infectious Diseases, full page: (LINK). Abstract, edited.]
The Lancet Infectious Diseases, Early Online Publication, 13 November 2013
doi:10.1016/S1473-3099(13)70286-X
Copyright ? 2013 Elsevier Ltd All rights reserved.
Pathogenesis of influenza-induced acute respiratory distress syndrome
Original Text
Kirsty R Short PhD a, Edwin J B Veldhuis Kroeze DVM a, Prof Ron A M Fouchier PhD a, Prof Thijs Kuiken PhD a
Summary
Acute respiratory distress syndrome (ARDS) is a fatal complication of influenza infection. In this Review we provide an integrated model for its pathogenesis. ARDS involves damage to the epithelial?endothelial barrier, fluid leakage into the alveolar lumen, and respiratory insufficiency. The most important part of the epithelial?endothelial barrier is the alveolar epithelium, strengthened by tight junctions. Influenza virus targets these epithelial cells, reducing sodium pump activity, damaging tight junctions, and killing infected cells. Infected epithelial cells produce cytokines that attract leucocytes?neutrophils and macrophages?and activate adjacent endothelial cells. Activated endothelial cells and infiltrated leucocytes stimulate further infiltration, and leucocytes induce production of reactive oxygen species and nitric oxide that damage the barrier. Activated macrophages also cause direct apoptosis of epithelial cells. This model for influenza-induced ARDS differs from the classic model, which is centred on endothelial damage, and provides a rationale for therapeutic intervention to moderate host response in influenza-induced ARDS.
________
a Department of Viroscience, Erasmus Medical Center, Rotterdam, Netherlands
Correspondence to: Prof Thijs Kuiken, Department of Viroscience, Erasmus Medical Center, Dr Molewaterplein 50, 3015GE Rotterdam, Zuid Holland, Netherlands
-
--------
The Lancet Infectious Diseases, Early Online Publication, 13 November 2013
doi:10.1016/S1473-3099(13)70286-X
Copyright ? 2013 Elsevier Ltd All rights reserved.
Pathogenesis of influenza-induced acute respiratory distress syndrome
Original Text
Kirsty R Short PhD a, Edwin J B Veldhuis Kroeze DVM a, Prof Ron A M Fouchier PhD a, Prof Thijs Kuiken PhD a
Summary
Acute respiratory distress syndrome (ARDS) is a fatal complication of influenza infection. In this Review we provide an integrated model for its pathogenesis. ARDS involves damage to the epithelial?endothelial barrier, fluid leakage into the alveolar lumen, and respiratory insufficiency. The most important part of the epithelial?endothelial barrier is the alveolar epithelium, strengthened by tight junctions. Influenza virus targets these epithelial cells, reducing sodium pump activity, damaging tight junctions, and killing infected cells. Infected epithelial cells produce cytokines that attract leucocytes?neutrophils and macrophages?and activate adjacent endothelial cells. Activated endothelial cells and infiltrated leucocytes stimulate further infiltration, and leucocytes induce production of reactive oxygen species and nitric oxide that damage the barrier. Activated macrophages also cause direct apoptosis of epithelial cells. This model for influenza-induced ARDS differs from the classic model, which is centred on endothelial damage, and provides a rationale for therapeutic intervention to moderate host response in influenza-induced ARDS.
________
a Department of Viroscience, Erasmus Medical Center, Rotterdam, Netherlands
Correspondence to: Prof Thijs Kuiken, Department of Viroscience, Erasmus Medical Center, Dr Molewaterplein 50, 3015GE Rotterdam, Zuid Holland, Netherlands
-
--------