August 23, 2010The Journal of Infectious DiseasesOpen Access

Influenza Virus–Cytokine‐Protease Cycle in the Pathogenesis of Vascular Hyperpermeability in Severe Influenza

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Structured PICO

Population

Weanling mice and cultured human umbilical vein endothelial cells

Intervention

Influenza A WSN/33(H1N1) virus infection, with or without transcriptional inhibitors, anti-cytokine antibodies, protease-activated receptor-2 antagonist, or trypsin inhibitor

Outcome

Vascular hyperpermeability, viral replication, and levels of proinflammatory cytokines (TNF-alpha, IL-6, IL-1beta) and trypsinsurrogate

The influenza virus-cytokine-protease cycle drives vascular hyperpermeability in severe influenza, which can be inhibited by targeting PAR-2 or trypsin.

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

Warrants testing of PAR-2 antagonists and trypsin inhibitors in severe influenza; animal data leave clinical translation open.

Cite This Study

Wang et al. (2010) studied this question.

synapsesocial.com/papers/6a7d3a8cb0b0e582d537d797 https://doi.org/10.1086/656044

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Influenza Virus–Cytokine‐Protease Cycle in the Pathogenesis of Vascular Hyperpermeability in Severe Influenza

Structured PICO

Discussion

Implication

Cite This Study

Influenza Virus–Cytokine‐Protease Cycle in the Pathogenesis of Vascular Hyperpermeability in Severe Influenza

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider