ArticleJournal of applied physiology (Bethesda, Md. : 1985)2011
Sources of alveolar soluble TNF receptors during acute lung injury of different etiologies.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Ventilator-induced Lung Injury Promotes Inflammation within the Pleural Cavity.American journal of respiratory cell and molecular biology · 2024Article
- Secreted Extracellular Cyclophilin A Is a Novel Mediator of Ventilator-induced Lung Injury.American journal of respiratory and critical care medicine · 2021Article
- Ventilation following established ARDS: a preclinical model framework to improve predictive power.Thorax · 2019Article
- ATP redirects cytokine trafficking and promotes novel membrane TNF signalingFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- In vivo compartmental analysis of leukocytes in mouse lungs.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Kinetic profiling of in vivo lung cellular inflammatory responses to mechanical ventilation.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- TNF-induced death signaling triggers alveolar epithelial dysfunction in acute lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Ventilation with "clinically relevant" high tidal volumes does not promote stretch-induced injury in the lungs of healthy mice.Critical care medicine · 2012Article
- Prevention of LPS-induced acute lung injury in mice by progranulin.Mediators of inflammation · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Elevated soluble tumor necrosis factor-α receptor (sTNFR) levels in bronchoalveolar lavage fluid (BALF) are associated with poor patient outcome in acute lung injury (ALI). The mechanisms underlying these increases are unknown, but it is possible that pulmonary inflammation and increased alveolar epithelial permeability may individually contribute. We investigated mechanisms of elevated BALF sTNFRs in two in vivo mouse models of ALI. Anesthetized mice were challenged with intratracheal lipopolysaccharide or subjected to injurious mechanical ventilation. Lipopolysaccharide instillation produced acute intra-alveolar inflammation, but minimal alveolar epithelial permeability changes, with increased BALF sTNFR p75, but not p55. Increased p75 levels were markedly attenuated by alveolar macrophage depletion. In contrast, injurious ventilation induced substantial alveolar epithelial permeability, with increased BALF p75 and p55, which strongly correlated with total protein. BALF sTNFRs were not increased in isolated buffer-perfused lungs (devoid of circulating sTNFRs) subjected to injurious ventilation. These results suggest that lipopolysaccharide-induced intra-alveolar inflammation upregulates alveolar macrophage-mediated production of sTNFR p75, whereas enhanced alveolar epithelial permeability following mechanical ventilation leads to increased BALF p75 and p55 via plasma leakage. These data provide new insights into differential regulation of intra-alveolar sTNFR levels during ALI and may suggest sTNFRs as potential markers for evaluating the pathophysiology of ALI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.