ArticleThe Journal of clinical investigation2016
Influenza leaves a TRAIL to pulmonary edema.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Influenza vaccination in patients with heart failure: comprehensive review of evidence, challenges, and clinical implications.Heart failure reviews · 2026Review
- The chemokine receptor CXCR3 promotes CD8Science advances · 2024Article
- The role of lung macrophages in acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Review
- Effect of an Adenovirus-Vectored Universal Influenza Virus Vaccine on Pulmonary Pathophysiology in a Mouse Model.Journal of virology · 2021Article
- Hypothesis: Pentoxifylline is a potential cytokine modulator therapeutic in COVID-19 patients.Pharmacology research & perspectives · 2020Review
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2 authors.
Funding
Abstract
Influenza infection can cause acute respiratory distress syndrome (ARDS), leading to poor disease outcome with high mortality. One of the driving features in the pathogenesis of ARDS is the accumulation of fluid in the alveoli, which causes severe pulmonary edema and impaired oxygen uptake. In this issue of the JCI, Peteranderl and colleagues define a paracrine communication between macrophages and type II alveolar epithelial cells during influenza infection where IFNα induces macrophage secretion of TRAIL that causes endocytosis of Na,K-ATPase by the alveolar epithelium. This reduction of Na,K-ATPase expression decreases alveolar fluid clearance, which in turn leads to pulmonary edema. Inhibition of the TRAIL signaling pathway has been shown to improve lung injury after influenza infection, and future studies will be needed to determine if blocking this pathway is a viable option in the treatment of ARDS.
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Registered trials
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