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Lancet Infect Dis. 2014 Jan;14(1):57-69. doi: 10.1016/S1473-3099(13)70286-X. Epub 2013 Nov 13.

Pathogenesis of influenza-induced acute respiratory distress syndrome.

Author information

1
Department of Viroscience, Erasmus Medical Center, Rotterdam, Netherlands.
2
Department of Viroscience, Erasmus Medical Center, Rotterdam, Netherlands. Electronic address: t.kuiken@erasmusmc.nl.

Abstract

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.

PMID:
24239327
DOI:
10.1016/S1473-3099(13)70286-X
[Indexed for MEDLINE]

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