ArticleThe Journal of clinical investigation1991
Eosinophil hematopoietins antagonize the programmed cell death of eosinophils. Cytokine and glucocorticoid effects on eosinophils maintained by endothelial cell-conditioned medium.
Article in The Journal of clinical investigation, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 154 citations in OpenAlex.
- Trial
- Defining and targeting mechanisms of eosinophilic inflammation in a new era of severe asthma treatment.The Journal of clinical investigation · 2024Review
- Recent advances of eosinophils and its correlated diseases.Frontiers in public health · 2022Review
- Article
- Targeting eosinophils in allergy, inflammation and beyond.Nature reviews. Drug discovery · 2013Review
- Article
- The treatment of vasomotor rhinitis with intranasal corticosteroids.The World Allergy Organization journal · 2009Article
- Effect of IL-5, glucocorticoid, and Fas ligation on Bcl-2 homologue expression and caspase activation in circulating human eosinophils.Clinical and experimental immunology · 2000Article
- Upregulation by glucocorticoids of responses to eosinopoietic cytokines in bone-marrow from normal and allergic mice.British journal of pharmacology · 2000Article
- Molecular biology and genetics of allergy and asthma.Archives of disease in childhood · 1998Review
- Review
- Theophylline accelerates human granulocyte apoptosis not via phosphodiesterase inhibition.The Journal of clinical investigation · 1997Article
- An interleukin 5 mutant distinguishes between two functional responses in human eosinophils.The Journal of experimental medicine · 1997Article
- Type 1 and type 2 cytokine dysregulation in human infectious, neoplastic, and inflammatory diseases.Clinical microbiology reviews · 1996Review
- Requirement of Lyn and Syk tyrosine kinases for the prevention of apoptosis by cytokines in human eosinophils.The Journal of experimental medicine · 1996Article
- Constitutive production of granulocyte/macrophage colony-stimulating factor by hypodense mononuclear eosinophils developed in vitro from hybrid eosinophil/basophil granulocytes.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Activation of the Fas receptor on lung eosinophils leads to apoptosis and the resolution of eosinophilic inflammation of the airways.The Journal of clinical investigation · 1995Article
- Differentiation in vitro of hybrid eosinophil/basophil granulocytes: autocrine function of an eosinophil developmental intermediate.The Journal of experimental medicine · 1995Article
- Th2 cells and cytokine networks in allergic inflammation of the lung.Mediators of inflammation · 1995Article
- Apoptosis and inflammation.Mediators of inflammation · 1995Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Granulocyte-macrophage colony-stimulating factor (GM-CSF) was established as the constitutive and elicited human umbilical vein endothelial cell-derived eosinophil viability-sustaining factor. Stimulation of endothelium cell monolayers with IL-1 alpha (5 U/ml) increased the 48-h elaboration of GM-CSF from a mean of 3.2 to a mean of 8.2 pM (P less than 0.05). Dexamethasone (100 nM) decreased the constitutive GM-CSF elaboration by 49% (P less than 0.001) but did not diminish production by IL-1 alpha-stimulated endothelium. However, eosinophil viability decreased by 21% in dexamethasone-pretreated IL-1 alpha-stimulated endothelial cell-conditioned medium (P less than 0.05), which suggested viability antagonism by glucocorticoids. After 24 h of culture, eosinophil viability for replicate cells in enriched medium alone or with 1 pM GM-CSF decreased from means of 43 and 75% to means of 21 and 54%, respectively, when dexamethasone was included (P less than 0.05). However, 10 pM GM-CSF, IL-3, or IL-5 protected the cells against dexamethasone and against endonuclease-specific DNA fragmentation. In this model system of eosinophil-tissue interactions, dexamethasone prevents the endothelial cells from inducing a pathobiologic phenotypic change in the eosinophil by suppression of GM-CSF elaboration to concentrations that are not cytoprotective. Cytokine priming by GM-CSF, IL-3, or IL-5 may account for the differential responsiveness of select eosinophilic disorders to glucocorticoids.
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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.