title: Influenza lung injury: mechanisms and therapeutic opportunities.
abstract: In this Perspectives, we discuss some recent developments in the pathogenesis of acute lung injury following influenza infection, with an emphasis on promising therapeutic leads. Damage to the alveolar-capillary barrier has been quantified in mice, and agents have been identified that can help to preserve barrier integrity, such as vasculotide, angiopoietin-like 4 neutralization, and sphingosine 1-phosphate mimics. Results from studies using mesenchymal stem cells have been disappointing, despite promising data in other types of lung injury. The roles of fatty acid binding protein 5, prostaglandin E2, and the interplay between IFN-γ and STAT1 in epithelial signaling during infection have been addressed in vitro. Finally, we discuss the role of autophagy in inflammatory cytokine production and the viral life cycle and the opportunities this presents for intervention.
authors.affiliation: Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard T. H. Chan School of Public Health.
authors.forename: David J
authors.initials: DJ
authors.lastname: Gregory
authors.affiliation: Molecular and Integrative Physiological Sciences Program, Department of Environmental Health, Harvard T. H. Chan School of Public Health lkobzik@hsph.harvard.edu.
authors.forename: Lester
authors.initials: L
authors.lastname: Kobzik
mesh_terms: D055371:Acute Lung Injury / Q000276:immunology / Q000378:metabolism / Q000821:virology*; D000818:Animals; D001343:Autophagy; D016207:Cytokines / Q000502:physiology; D004848:Epithelium / Q000473:pathology / Q000821:virology; D006801:Humans; D007251:Influenza, Human / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D008168:Lung / Q000378:metabolism / Q000473:pathology* / Q000821:virology; D020545:Respiratory Mucosa / Q000473:pathology / Q000821:virology; D015398:Signal Transduction
chemical_list: D016207:Cytokines
keywords: acute lung injury; autophagy; influenza; signaling