| pubmed-article:11859139 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11859139 | lifeskim:mentions | umls-concept:C0021759 | lld:lifeskim |
| pubmed-article:11859139 | lifeskim:mentions | umls-concept:C0014467 | lld:lifeskim |
| pubmed-article:11859139 | lifeskim:mentions | umls-concept:C0014876 | lld:lifeskim |
| pubmed-article:11859139 | lifeskim:mentions | umls-concept:C0033414 | lld:lifeskim |
| pubmed-article:11859139 | lifeskim:mentions | umls-concept:C0599896 | lld:lifeskim |
| pubmed-article:11859139 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:11859139 | pubmed:dateCreated | 2002-2-22 | lld:pubmed |
| pubmed-article:11859139 | 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. | lld:pubmed |
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| pubmed-article:11859139 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11859139 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11859139 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:11859139 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11859139 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:11859139 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:11859139 | pubmed:author | pubmed-author:MishraAnilA | lld:pubmed |
| pubmed-article:11859139 | pubmed:author | pubmed-author:HoganSimon... | lld:pubmed |
| pubmed-article:11859139 | pubmed:author | pubmed-author:BrandtEric... | lld:pubmed |
| pubmed-article:11859139 | pubmed:author | pubmed-author:RothenbergMar... | lld:pubmed |
| pubmed-article:11859139 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11859139 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11859139 | pubmed:volume | 168 | lld:pubmed |
| pubmed-article:11859139 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11859139 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11859139 | pubmed:pagination | 2464-9 | lld:pubmed |
| pubmed-article:11859139 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11859139 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:11859139 | pubmed:articleTitle | IL-5 promotes eosinophil trafficking to the esophagus. | lld:pubmed |
| pubmed-article:11859139 | pubmed:affiliation | Division of Allergy and Immunology, Department of Pediatrics, Children's Hospital Medical Center, Cincinnati, OH 45229, USA. | lld:pubmed |
| pubmed-article:11859139 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11859139 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:11859139 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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