ArticleThe Journal of experimental medicine1990
Tumor necrosis factor alpha/cachectin stimulates eosinophil oxidant production and toxicity towards human endothelium.
Article in The Journal of experimental medicine, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 145 citations in OpenAlex.
- Inflammatory profile of eosinophils in asthma-COPD overlap and eosinophilic COPD: a multi-omics study.Frontiers in immunology · 2024Article
- Idiopathic hypereosinophilic syndrome with hepatic sinusoidal obstruction syndrome: A case report and literature review.World journal of gastrointestinal surgery · 2023Article
- Dapsone-induced DRESS after infliximab-induced vasculitis: a case of cerebral infarction in the context of multiple drug reactions.BMJ case reports · 2020Article
- Comparative gene expression analysis ofInternational journal of reproductive biomedicine · 2020Article
- Macmoondongtang modulates Th1-/Th2-related cytokines and alleviates asthma in a murine model.PloS one · 2019Article
- Portal Vein Thrombosis and Thrombocytopenia in Eosinophilic Granulomatosis with Polyangiitis: A Paradox?European journal of case reports in internal medicine · 2018Article
- The significance of eosinophils in predicting the severity of acute ischemic stroke.Oncotarget · 2017Article
- Hemodynamic and Hematologic Effects of Histotripsy of Free-Flowing Blood: Implications for Ultrasound-Mediated Thrombolysis.Journal of vascular and interventional radiology : JVIR · 2015Article
- Acute cerebral infarction in watershed distribution in a patient with hypereosinophilic syndrome without cardiac lesion.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014Article
- Eosinophil cytokines, chemokines, and growth factors: emerging roles in immunity.Frontiers in immunology · 2014Review
- SOCS3 dictates the transition of divergent time-phased events in granulocyte TNF-α signaling.Cellular & molecular immunology · 2014Article
- Article
- Heparin and related drugs: beyond anticoagulant activity.ISRN pharmacology · 2013Article
- Multiple cerebral infarctions related to famotidine-induced eosinophilia.Journal of neurology · 2012Article
- Differential oxidative stress gene expression profile in mouse brain after proton exposure.In vitro cellular & developmental biology. Animal · 2010Article
- Decrease in airway mucous gene expression caused by treatment with anti-tumor necrosis factor alpha in a murine model of allergic asthma.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2009Article
- The soluble tumor necrosis factor-alpha receptor suppresses airway inflammation in a murine model of acute asthma.Yonsei medical journal · 2009Article
- Eosinophilia and first-line coagulation testing.Journal of thrombosis and thrombolysis · 2009Article
- Targeting TNF-alpha: a novel therapeutic approach for asthma.The Journal of allergy and clinical immunology · 2008Review
- Increased number of apoptotic endothelial cells in bladder of interstitial cystitis patients.World journal of urology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Eosinophils (EOs) participate in a variety of inflammatory states characterized by endothelial cell damage, such as vasculitis, pneumonitis, and endocarditis. We find that 100 U/ml TNF-alpha/cachectin (TNF), a concentration attainable in the blood of humans with parasitic infestations, stimulates highly purified populations of EOs to damage human umbilical vein endothelial cells (HUVEC), a model of human endothelium. This TNF-dependent EO cytotoxicity is strongly inhibited by heparin and methyprednisolone but unaffected by the platelet-activating factor antagonist BN52012 or scavengers of superoxide anion and H2O2, superoxide dismutase and catalase. However, addition of a physiologically relevant concentration of Br- (100 microM) enhances EO/TNF damage to HUVEC, implicating the possible participation of EO peroxidase (EPO) in the killing mechanism. EOs adherent to FCS-coated plastic wells more than double their production of superoxide anion and the cytotoxic EPO-derived oxidant HOBr when exposed to TNF, showing that TNF activates the respiratory burst of EOs attached to a "physiologic" surface. Unlike PMNs, EOs were not irreversibly activated to kill unopsonized endothelium by previous exposure to TNF, and did not degranulate or upregulate CR3 expression as detected by Mo1 in the presence of 100 U/ml TNF. HUVEC exposed 18 h to TNF were considerably more susceptible to lysis by PMA-activated EOs and reagent H2O2, demonstrating a direct effect of TNF upon endothelium, perhaps through inhibition of antioxidant defenses. These findings suggest that abnormally elevated serum levels of TNF may provoke EOs to damage endothelial cells and thereby play a role in the pathogenesis of tissue damage in hypereosinophilic states.
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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.