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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1994-3-30
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pubmed:abstractText |
Hematopoietins, interleukin (IL)-3, IL-5, and granulocyte/macrophage colony-stimulating factor (GM-CSF) have previously been shown to prolong eosinophil survival and abrogate apoptosis. The objective of this study was to investigate the effect of transforming growth factor beta (TGF-beta) on eosinophil survival and apoptosis. Eosinophils from peripheral blood of mildly eosinophilic donors were isolated to > 97% purity using discontinuous Percoll density gradient. Eosinophils were cultured with hematopoietins with or without TGF-beta for 4 d and their viability was assessed. We confirmed previous observations that hematopoietins prolonged eosinophil survival and inhibited apoptosis. TGF-beta at concentrations > or = 10(-12) M abrogated the survival-prolonging effects of hematopoietins in a dose-dependent manner and induced apoptosis as determined by DNA fragmentation in agarose gels. The effect of TGF-beta was blocked by an anti-TGF-beta antibody. The anti-TGF-beta antibody also prolonged eosinophil survival on its own. The culture of eosinophils with IL-3 and GM-CSF stimulated the synthesis of GM-CSF and IL-5, respectively, suggesting an autocrine mechanism of growth factor production. TGF-beta inhibited the synthesis of GM-CSF and IL-5 by eosinophils. TGF-beta did not have any effect on the expression of GM-CSF receptors on eosinophils. We also studied the effect of TGF-beta on eosinophil function and found that TGF-beta inhibited the release of eosinophil peroxidase. Thus, TGF-beta seems to inhibit eosinophil survival and function. The inhibition of endogenous synthesis of hematopoietins may be one mechanism by which TGF-beta blocks eosinophil survival and induces apoptosis.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1379084,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1387670,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1401075,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1569205,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1588044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1608949,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1726704,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1726708,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1730922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1752957,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1875171,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1875172,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1919039,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-1940348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2008184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2230651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2460564,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2478145,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2506282,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2521375,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2526691,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2550928,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-2787531,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-3133397,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-3840509,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-6252099,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-6878618,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8113672-7682241
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1007
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
179
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1041-5
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8113672-Antibodies, Monoclonal,
pubmed-meshheading:8113672-Apoptosis,
pubmed-meshheading:8113672-Cell Survival,
pubmed-meshheading:8113672-Cells, Cultured,
pubmed-meshheading:8113672-Eosinophilia,
pubmed-meshheading:8113672-Eosinophils,
pubmed-meshheading:8113672-Granulocyte-Macrophage Colony-Stimulating Factor,
pubmed-meshheading:8113672-Hematopoietic Cell Growth Factors,
pubmed-meshheading:8113672-Humans,
pubmed-meshheading:8113672-Hypersensitivity,
pubmed-meshheading:8113672-Interleukin-3,
pubmed-meshheading:8113672-Interleukin-5,
pubmed-meshheading:8113672-Kinetics,
pubmed-meshheading:8113672-Reference Values,
pubmed-meshheading:8113672-Transforming Growth Factor beta
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pubmed:year |
1994
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pubmed:articleTitle |
Transforming growth factor beta abrogates the effects of hematopoietins on eosinophils and induces their apoptosis.
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pubmed:affiliation |
University of Texas Medical Branch, Department of Internal Medicine, Galveston 77555-0762.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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