| pubmed-article:16495517 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16495517 | lifeskim:mentions | umls-concept:C0021759 | lld:lifeskim |
| pubmed-article:16495517 | lifeskim:mentions | umls-concept:C0214743 | lld:lifeskim |
| pubmed-article:16495517 | lifeskim:mentions | umls-concept:C0239946 | lld:lifeskim |
| pubmed-article:16495517 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:16495517 | lifeskim:mentions | umls-concept:C0449258 | lld:lifeskim |
| pubmed-article:16495517 | lifeskim:mentions | umls-concept:C1998811 | lld:lifeskim |
| pubmed-article:16495517 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16495517 | pubmed:dateCreated | 2006-2-23 | lld:pubmed |
| pubmed-article:16495517 | pubmed:abstractText | Eosinophils are frequently found in increased numbers in a variety of chronic fibrotic diseases; however, their role in the development of hepatic fibrosis has not been dissected in vivo. Here, we used interleukin-5 (IL-5) knockout (KO) mice to determine whether eosinophils contribute to the progressive liver fibrosis that develops in response to chronic Schistosoma mansoni infection. Although infection intensities were similar in C57BL/6 and IL-5 KO mice, the average size of granulomas was significantly smaller in both acutely and chronically infected IL-5 KO mice. Their granulomas were also completely devoid of eosinophils. In addition, the knockout mice displayed over a 40% reduction in hepatic fibrosis by week 16 postinfection. The reduced fibrosis was associated with increased production of the antifibrotic cytokine gamma interferon. Moreover, although IL-13 production did not decrease consistently in the absence of IL-5, IL-13-triggered responses were substantially reduced in the granulomatous tissues. This was confirmed by analyzing the expression of several genes associated with alternative macrophage activation, including arginase 1, Fizz-1, and YM-1. Importantly, all of these IL-13-regulated genes have been linked with the mechanisms of wound healing and fibrosis. In addition to IL-5 polarizing the antigen-specific CD4+ Th2 cell response, we found that granuloma eosinophils were themselves a significant source of IL-13. Thus, by producing profibrotic mediators and polarizing the Th2 response, these findings illustrate both direct and indirect roles for eosinophils and IL-5 in the pathogenesis of schistosomiasis-induced liver fibrosis. Thus, inhibiting the activity of IL-5 or eosinophils may prove effective for a variety of chronic fibrotic diseases. | lld:pubmed |
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| pubmed-article:16495517 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16495517 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16495517 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16495517 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16495517 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:16495517 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:WynnThomas... | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:FengCarl GCG | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:ThompsonRober... | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:CheeverAllen... | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:RosenbergHele... | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:ReimanRachael... | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:HariDanielleD | lld:pubmed |
| pubmed-article:16495517 | pubmed:author | pubmed-author:KnightRachelR | lld:pubmed |
| pubmed-article:16495517 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16495517 | pubmed:volume | 74 | lld:pubmed |
| pubmed-article:16495517 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16495517 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16495517 | pubmed:pagination | 1471-9 | lld:pubmed |
| pubmed-article:16495517 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:16495517 | pubmed:meshHeading | pubmed-meshheading:16495517... | lld:pubmed |
| pubmed-article:16495517 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16495517 | pubmed:articleTitle | Interleukin-5 (IL-5) augments the progression of liver fibrosis by regulating IL-13 activity. | lld:pubmed |
| pubmed-article:16495517 | pubmed:affiliation | Immunopathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892-8003, USA. | lld:pubmed |
| pubmed-article:16495517 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16495517 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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