AI Article Synopsis
- Recent studies focus on the causes of acute lung injury from influenza and highlight potential treatments that protect the alveolar-capillary barrier.
- Researchers have identified specific agents, such as vasculotide and sphingosine 1-phosphate mimics, that may help maintain barrier integrity, although mesenchymal stem cells show less promise for lung injuries.
- The review also explores the roles of various proteins and signaling pathways in lung epithelial response to infection, as well as the impact of autophagy on inflammation and the virus, suggesting new avenues for therapeutic intervention.
Article 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4652148 | PMC |
| http://dx.doi.org/10.1152/ajplung.00283.2015 | DOI Listing |
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