| pubmed-article:10464058 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10464058 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:10464058 | lifeskim:mentions | umls-concept:C0014597 | lld:lifeskim |
| pubmed-article:10464058 | lifeskim:mentions | umls-concept:C0009506 | lld:lifeskim |
| pubmed-article:10464058 | lifeskim:mentions | umls-concept:C0021853 | lld:lifeskim |
| pubmed-article:10464058 | lifeskim:mentions | umls-concept:C0149784 | lld:lifeskim |
| pubmed-article:10464058 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:10464058 | lifeskim:mentions | umls-concept:C0547047 | lld:lifeskim |
| pubmed-article:10464058 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:10464058 | pubmed:dateCreated | 1999-11-19 | lld:pubmed |
| pubmed-article:10464058 | pubmed:abstractText | Interleukin-1beta (IL-1beta) increases the production of complement component C3 in enterocytes. Heat shock regulates the response to cytokines and other inflammatory mediators in various cell types. We tested the hypothesis that the heat-shock response regulates IL-1beta-induced C3 production in the enterocyte. Cultured Caco-2 cells, a human intestinal epithelial cell line, were treated with sodium arsenite (10-500 microM) for 1 h or subjected to hyperthermia (43 degrees C) for 1-4 h, and allowed to recover for 1 h. The cells were then treated with IL-1beta (0.5 ng/ml) for up to 24 h, whereafter C3 levels were measured by ELISA and C3 mRNA by Northern blot analysis. Heat-shock protein of 72 kDa (hsp72) was determined by Western blot analysis. Treatment of the cells with sodium arsenite or subjecting them to hyperthermia induced the expression of hsp72. The IL-1beta-induced expression of C3 mRNA and C3 production were down-regulated by hyperthermia and sodium arsenite in a dose-dependent fashion. The results suggest that the stress response induced by hyperthermia or sodium arsenite decreases IL-1beta-induced C3 production in human enterocytes. | lld:pubmed |
| pubmed-article:10464058 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10464058 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10464058 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10464058 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:10464058 | pubmed:issn | 0143-5221 | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:FischerJ EJE | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:REESW AWA | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:MoléLL | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:HasselgrenP... | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:SalzmanA LAL | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:ParikhA AAA | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:WongH RHR | lld:pubmed |
| pubmed-article:10464058 | pubmed:author | pubmed-author:PrittsT ATA | lld:pubmed |
| pubmed-article:10464058 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10464058 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10464058 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10464058 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10464058 | pubmed:pagination | 331-7 | lld:pubmed |
| pubmed-article:10464058 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:10464058 | pubmed:meshHeading | pubmed-meshheading:10464058... | lld:pubmed |
| pubmed-article:10464058 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10464058 | pubmed:articleTitle | Stress response decreases the interleukin-1beta-induced production of complement component C3 in human intestinal epithelial cells. | lld:pubmed |
| pubmed-article:10464058 | pubmed:affiliation | Department of Surgery, University of Cincinnati Medical Center, Cincinnati, OH 45267, USA. | lld:pubmed |
| pubmed-article:10464058 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10464058 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10464058 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:10464058 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:10464058 | lld:pubmed |
