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| pubmed-article:8112867 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:8112867 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:8112867 | lifeskim:mentions | umls-concept:C0079633 | lld:lifeskim |
| pubmed-article:8112867 | lifeskim:mentions | umls-concept:C0376618 | lld:lifeskim |
| pubmed-article:8112867 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:8112867 | lifeskim:mentions | umls-concept:C2612728 | lld:lifeskim |
| pubmed-article:8112867 | lifeskim:mentions | umls-concept:C1515926 | lld:lifeskim |
| pubmed-article:8112867 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:8112867 | pubmed:dateCreated | 1994-3-30 | lld:pubmed |
| pubmed-article:8112867 | pubmed:abstractText | Interleukin-8 (IL-8), a neutrophil chemoattractant and activating cytokine, has been implicated as a proinflammatory mediator in gram-negative sepsis. In vitro data support the notion of IL-8 as an endothelial adherence inhibitor. To evaluate this issue, we infused six volunteers with reference endotoxin and measured plasma levels of IL-8, neutrophil tumor necrosis factor alpha (TNF-alpha) receptors, TNF-alpha-induced adherence to fibronectin, and neutrophil chemotaxis to IL-8 and other attractants. We found that, at 3 h postinfusion, IL-8 but not TNF-alpha plasma levels were elevated. Neutrophils had shed L-selectin (mean channel fluorescence decrease, 79 +/- 9 to 49 +/- 7; P = 0.0625) and TNF-alpha receptors (decrease in number of receptors per cell, 1,596 +/- 340 to 574 +/- 93; P = 0.004). Cells were chemotactically desensitized to IL-8. TNF-alpha-induced adherence to fibronectin was suppressed from 69% +/- 5% of the phorbol myristate acetate response to 38% +/- 7% (P = 0.0154). These findings support the notion that release of IL-8 into the vascular space may be an in vivo mechanism for suppression of neutrophil accumulation at extravascular sites. L-Selectin loss would reduce the ability of neutrophils to adhere to activated endothelial cells. The specific loss of migratory response to IL-8 would impair neutrophil delivery to areas where IL-8 was the predominant chemoattractant. Loss of TNF-alpha-induced adherence to fibronectin would blunt those responses, including production of oxidants, capacitated by adherence. | lld:pubmed |
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| pubmed-article:8112867 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8112867 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8112867 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8112867 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8112867 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:8112867 | pubmed:issn | 0019-9567 | lld:pubmed |
| pubmed-article:8112867 | pubmed:author | pubmed-author:BabcockG FGF | lld:pubmed |
| pubmed-article:8112867 | pubmed:author | pubmed-author:BjornsonH SHS | lld:pubmed |
| pubmed-article:8112867 | pubmed:author | pubmed-author:SolomkinJ SJS | lld:pubmed |
| pubmed-article:8112867 | pubmed:author | pubmed-author:BUCHF LFL | lld:pubmed |
| pubmed-article:8112867 | pubmed:author | pubmed-author:TindalC JCJ | lld:pubmed |
| pubmed-article:8112867 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8112867 | pubmed:volume | 62 | lld:pubmed |
| pubmed-article:8112867 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8112867 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8112867 | pubmed:pagination | 943-7 | lld:pubmed |
| pubmed-article:8112867 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:8112867 | pubmed:meshHeading | pubmed-meshheading:8112867-... | lld:pubmed |
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| pubmed-article:8112867 | pubmed:meshHeading | pubmed-meshheading:8112867-... | lld:pubmed |
| pubmed-article:8112867 | pubmed:meshHeading | pubmed-meshheading:8112867-... | lld:pubmed |
| pubmed-article:8112867 | pubmed:meshHeading | pubmed-meshheading:8112867-... | lld:pubmed |
| pubmed-article:8112867 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8112867 | pubmed:articleTitle | Alterations of neutrophil responses to tumor necrosis factor alpha and interleukin-8 following human endotoxemia. | lld:pubmed |
| pubmed-article:8112867 | pubmed:affiliation | Department of Surgery, University of Cincinnati College of Medicine, Ohio. | lld:pubmed |
| pubmed-article:8112867 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8112867 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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