| pubmed-article:12041508 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12041508 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:12041508 | lifeskim:mentions | umls-concept:C0021753 | lld:lifeskim |
| pubmed-article:12041508 | lifeskim:mentions | umls-concept:C0023810 | lld:lifeskim |
| pubmed-article:12041508 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:12041508 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12041508 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:12041508 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:12041508 | pubmed:dateCreated | 2002-5-31 | lld:pubmed |
| pubmed-article:12041508 | pubmed:abstractText | Endotoxin or lipopolysaccharide (LPS) tolerance may be partially due to the secretion of potent anti-inflammatory cytokines following severe Gram-negative infections, or by low doses of LPS. In this work, we describe the effects of interleukin-1 (IL-1) and tumour necrosis factor alpha (TNF-), two early cytokines secreted after LPS exposure, in the induction of LPS tolerance. Our results demonstrate that mice treated with three daily doses of 100 ng of IL-1 were tolerant to LPS-induced shock. However, TNF- was unable to induce an LPS refractory state. Given the fact that 100 ng of IL-1 increase the plasma levels of glucocorticoids, we evaluated whether a daily injection of dexamethasone (DEX) alone was able to reproduce the LPS-like tolerant state. However, no signs of LPS refractoriness were detected, except when DEX was administered concomitantly with a dose of IL-1 that does not induce corticosterone secretion (12 ng/mouse). This dose was found to induce in vitro up-regulation of the glucocorticoid receptors (GcR) of peritoneal macrophages following 24 h of treatment. In addition, we demonstrate that IL-1 is capable of inducing the down-regulation of Toll-like receptor 4 (TLR4), a crucial molecule in the signal transduction of LPS. Taken together, our results indicate that IL-1 can generate tolerance to LPS in vivo, and suggest that the regulation of mechanisms of the down-regulation of TLR4, as well as those involved in the expression of GcR and/or in the secretion of glucocorticoids, would be crucial for these effects. | lld:pubmed |
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| pubmed-article:12041508 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12041508 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12041508 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12041508 | pubmed:month | May | lld:pubmed |
| pubmed-article:12041508 | pubmed:issn | 0009-9104 | lld:pubmed |
| pubmed-article:12041508 | pubmed:author | pubmed-author:FernándezGG | lld:pubmed |
| pubmed-article:12041508 | pubmed:author | pubmed-author:IsturizM AMA | lld:pubmed |
| pubmed-article:12041508 | pubmed:author | pubmed-author:PalermoMM | lld:pubmed |
| pubmed-article:12041508 | pubmed:author | pubmed-author:VulcanoMM | lld:pubmed |
| pubmed-article:12041508 | pubmed:author | pubmed-author:Alves-RosaFF | lld:pubmed |
| pubmed-article:12041508 | pubmed:author | pubmed-author:Beigier-Bompa... | lld:pubmed |
| pubmed-article:12041508 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12041508 | pubmed:volume | 128 | lld:pubmed |
| pubmed-article:12041508 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12041508 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12041508 | pubmed:pagination | 221-8 | lld:pubmed |
| pubmed-article:12041508 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:12041508 | pubmed:meshHeading | pubmed-meshheading:12041508... | lld:pubmed |
| pubmed-article:12041508 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12041508 | pubmed:articleTitle | Interleukin-1beta induces in vivo tolerance to lipopolysaccharide in mice. | lld:pubmed |
| pubmed-article:12041508 | pubmed:affiliation | División Immunología, Instituto de Investigaciones Hematológicas, Academia Nacional de Medicina, Buenos Aires, Argentina. ferar@ciudad.com.ar | lld:pubmed |
| pubmed-article:12041508 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12041508 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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