| pubmed-article:12379683 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12379683 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:12379683 | lifeskim:mentions | umls-concept:C0010132 | lld:lifeskim |
| pubmed-article:12379683 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
| pubmed-article:12379683 | lifeskim:mentions | umls-concept:C0014264 | lld:lifeskim |
| pubmed-article:12379683 | lifeskim:mentions | umls-concept:C0036974 | lld:lifeskim |
| pubmed-article:12379683 | lifeskim:mentions | umls-concept:C1327413 | lld:lifeskim |
| pubmed-article:12379683 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:12379683 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:12379683 | pubmed:dateCreated | 2002-10-15 | lld:pubmed |
| pubmed-article:12379683 | pubmed:abstractText | Corticotropin-releasing hormone (CRH) exerts an anti-inflammatory effect indirectly, via cortisole production, and a proinflammatory effect directly on immune cells. The aim of the present work was to examine the effect of CRH on macrophage-derived cytokines both in vitro and in vivo. For the in vitro experiments we used two types of macrophages: (i) the RAW264.7 monocyte/macrophage cell line and (ii) thioglycolate-elicited peritoneal macrophages from BALB/c mice. We have found that CRH enhanced lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-alpha), interleukin-1beta (IL-1beta), and IL-6 production. For the in vivo experiments we have used the LPS-induced endotoxin shock model in BALB/c mice, an established model for systemic inflammation in which macrophages are the major source of the proinflammatory cytokines responsible for the development of the shock. Administration of antalarmin, a synthetic CRH receptor 1 (CRHR1) antagonist, prior to LPS prolonged survival in a statistically significant manner. The effect was more evident at the early stages of endotoxin shock. CRHR1 blockade suppressed LPS-induced elevation of the macrophage-derived cytokines TNF-alpha, IL-1beta, and IL-6, confirming the role of CRH signals in cytokine expression. In conclusion, our data suggest that CRH signals play an early and crucial role in augmenting LPS-induced proinflammatory cytokine production by macrophages. Our data suggest that the diffuse neuroendocrine system via CRH directly affects the immune system at the level of macrophage activation and cytokine production. | lld:pubmed |
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| pubmed-article:12379683 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12379683 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12379683 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12379683 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12379683 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:12379683 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:12379683 | pubmed:author | pubmed-author:TsatsanisChri... | lld:pubmed |
| pubmed-article:12379683 | pubmed:author | pubmed-author:GravanisAchil... | lld:pubmed |
| pubmed-article:12379683 | pubmed:author | pubmed-author:MargiorisAndr... | lld:pubmed |
| pubmed-article:12379683 | pubmed:author | pubmed-author:AgelakiSofiaS | lld:pubmed |
| pubmed-article:12379683 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12379683 | pubmed:volume | 70 | lld:pubmed |
| pubmed-article:12379683 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12379683 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12379683 | pubmed:pagination | 6068-74 | lld:pubmed |
| pubmed-article:12379683 | pubmed:dateRevised | 2010-9-14 | lld:pubmed |
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| pubmed-article:12379683 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12379683 | pubmed:articleTitle | Corticotropin-releasing hormone augments proinflammatory cytokine production from macrophages in vitro and in lipopolysaccharide-induced endotoxin shock in mice. | lld:pubmed |
| pubmed-article:12379683 | pubmed:affiliation | Deparment of Clinical Chemistry-Biochemistry, School of Medicine, University of Crete, Heraklion, Crete, Greece. | lld:pubmed |
| pubmed-article:12379683 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12379683 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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