ArticleJournal of vascular research2016
Gram-Negative Pneumonia Alters Large-Vein Cell-Adhesion Molecule Profile and Potentiates Experimental Stasis Venous Thrombosis.
Article in Journal of vascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
The trial behind it
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
7 citing papers in PubMed, 8 citations in OpenAlex.
- P- and E- selectin in venous thrombosis and non-venous pathologies.Journal of thrombosis and haemostasis : JTH · 2022Review
- Identification of genes, pathways and transcription factor-miRNA-target gene networks and experimental verification in venous thromboembolism.Scientific reports · 2021Article
- TLR3 absence confers increased survival with improved macrophage activity against pneumonia.JCI insight · 2019Article
- Direct pulmonary delivery of solubilized curcumin reduces severity of lethal pneumonia.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Sepsis-induced thrombus formation and cell-specific HIFs.Thrombosis research · 2018Article
- Immune Factors in Deep Vein Thrombosis Initiation.Trends in immunology · 2018Review
- The association of venous thromboembolism chemoprophylaxis timing on venous thromboembolism after major vascular surgery.Journal of vascular surgery · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND/
aimsPneumonia is a significant risk factor for the development of venous thrombosis (VT). Cell-adhesion molecules (CAMs) are linked to the pathogenesis of both pneumonia and VT. We hypothesized that remote infection would confer a prothrombogenic milieu via systemic elevation of CAMs.
methodsLung injury was induced in wild-type (C57BL/6) mice by lung contusion or intratracheal inoculation with Klebsiella pneumoniae or saline controls. K. pneumoniae-treated mice and controls additionally underwent inferior vena cava (IVC) ligation to generate VT.
resultsLung-contusion mice demonstrated no increase in E-selectin or P-selectin whereas mice infected with K. pneumoniae demonstrated increased circulating P-selectin, ICAM-1, VCAM-1 and thrombin-antithrombin (TAT) complexes. Mice with pneumonia formed VT 3 times larger than controls, demonstrated significantly more upregulation of vein-wall and systemic CAMs, and formed erythrocyte-rich thrombi.
conclusionElevated CAM expression was identified in mice with pneumonia, but not lung contusion, indicating that the type of inflammatory stimulus and the presence of infection drive the vein-wall response. Elevation of CAMs was associated with amplified VT and may represent an alternate mechanism by which to target the prevention of VT.
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What OpenQuestion holds
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.