Source:http://linkedlifedata.com/resource/pubmed/id/11859139
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2002-2-22
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pubmed:abstractText |
Eosinophil infiltration into the esophagus occurs in a wide range of diseases; however, the underlying pathophysiological mechanisms involved are largely unknown. We now report that the Th2 cytokine, IL-5, is necessary and sufficient for the induction of eosinophil trafficking to the esophagus. We show that transgenic mice overexpressing IL-5 under the control of a T cell (CD2) or a small intestinal enterocyte (fatty acid-binding protein) promoter have markedly increased eosinophil numbers in the esophagus. For example, esophageal eosinophil levels are 1.9 +/- 0.9 and 121 +/- 14 eosinophils/mm(2) in wild-type and CD2-IL-5-transgenic mice, respectively. Consistent with this effect being mediated by a systemic mechanism, pharmacological administration of IL-5 via a miniosmotic pump in the peritoneal cavity resulted in blood and esophageal eosinophilia. To examine the role of IL-5 in oral Ag-induced esophageal eosinophilia, eosinophilic esophagitis was induced by allergen exposure in IL-5-deficient and wild-type mice. Importantly, IL-5-deficient mice were resistant to eosinophilic esophagitis. Finally, we examined the role of eotaxin when IL-5 was overproduced in vivo. Esophageal eosinophil levels in CD2-IL-5-transgenic mice were found to decrease 15-fold in the absence of the eotaxin gene; however, esophageal eosinophil numbers in eotaxin-deficient IL-5-transgenic mice still remained higher than wild-type mice. In conclusion, these studies demonstrate a central role for IL-5 in inducing eosinophil trafficking to the esophagus.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD2,
http://linkedlifedata.com/resource/pubmed/chemical/Ccl11 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL11,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-5,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
168
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2464-9
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:11859139-Administration, Oral,
pubmed-meshheading:11859139-Animals,
pubmed-meshheading:11859139-Antigens, CD2,
pubmed-meshheading:11859139-Chemokine CCL11,
pubmed-meshheading:11859139-Chemokines, CC,
pubmed-meshheading:11859139-Chemotaxis, Leukocyte,
pubmed-meshheading:11859139-Eosinophilia,
pubmed-meshheading:11859139-Eosinophils,
pubmed-meshheading:11859139-Esophagitis,
pubmed-meshheading:11859139-Esophagus,
pubmed-meshheading:11859139-Interleukin-5,
pubmed-meshheading:11859139-Intestine, Small,
pubmed-meshheading:11859139-Mice,
pubmed-meshheading:11859139-Mice, Inbred BALB C,
pubmed-meshheading:11859139-Mice, Transgenic,
pubmed-meshheading:11859139-Ovalbumin,
pubmed-meshheading:11859139-Promoter Regions, Genetic
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pubmed:year |
2002
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pubmed:articleTitle |
IL-5 promotes eosinophil trafficking to the esophagus.
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pubmed:affiliation |
Division of Allergy and Immunology, Department of Pediatrics, Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
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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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