| pubmed-article:3968867 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:3968867 | lifeskim:mentions | umls-concept:C0014257 | lld:lifeskim |
| pubmed-article:3968867 | lifeskim:mentions | umls-concept:C0027950 | lld:lifeskim |
| pubmed-article:3968867 | lifeskim:mentions | umls-concept:C0030054 | lld:lifeskim |
| pubmed-article:3968867 | lifeskim:mentions | umls-concept:C1947912 | lld:lifeskim |
| pubmed-article:3968867 | lifeskim:mentions | umls-concept:C0872351 | lld:lifeskim |
| pubmed-article:3968867 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:3968867 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:3968867 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:3968867 | pubmed:dateCreated | 1985-3-13 | lld:pubmed |
| pubmed-article:3968867 | pubmed:abstractText | We have measured the effect of activated neutrophils on endothelial monolayer integrity in vitro by assessing the capacity of endothelial monolayers on polycarbonate filters to exclude 125I-albumin. Although formylmethionyl-leucyl-phenylalanine (FMLP)-activated neutrophils failed to induce 51Cr-release or detachment after 4 hours of incubation with endothelial monolayers cultured in polystyrene wells, FMLP-activated neutrophils produced a marked increase in the passage of 125I-albumin across bovine aortic or pulmonary artery endothelial monolayers on polycarbonate filters. This effect was evident as early as 30 minutes following the addition of FMLP-activated neutrophils to the monolayer and reached 180% over control values at 2 hours (p = 0.001). Light and transmission electron microscopic examination of the polycarbonate filters exposed to FMLP-activated neutrophils revealed focal disruption of the endothelial monolayers. Chronic granulomatous disease neutrophils produced similar disruption of the endothelial monolayer at 2 hours. Moreover, catalase and superoxide dismutase failed to reduce significantly the neutrophil-mediated increase in 125I-albumin passage at 2 hours. Cell-free postsecretory supernatants of FMLP-activated neutrophils, leukotriene C4, and platelet activating factor did not induce a significant increase in 125I-albumin passage across the endothelial monolayers. Of note, FMLP-activated neutrophils from a patient with a congenital abnormality of neutrophil adhesion and chemotaxis did not induce disruption of the monolayer or increase 125I-albumin passage. We conclude that activated neutrophils mediate rapid, nonlytic disruption of endothelial monolayer integrity by an oxygen radical-independent mechanism that requires neutrophil-endothelial contact. | lld:pubmed |
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| pubmed-article:3968867 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:3968867 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:3968867 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:3968867 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:3968867 | pubmed:issn | 0023-6837 | lld:pubmed |
| pubmed-article:3968867 | pubmed:author | pubmed-author:HarkerL ALA | lld:pubmed |
| pubmed-article:3968867 | pubmed:author | pubmed-author:ReidyM AMA | lld:pubmed |
| pubmed-article:3968867 | pubmed:author | pubmed-author:OchsH DHD | lld:pubmed |
| pubmed-article:3968867 | pubmed:author | pubmed-author:SchwartzS MSM | lld:pubmed |
| pubmed-article:3968867 | pubmed:author | pubmed-author:HarlanJ MJM | lld:pubmed |
| pubmed-article:3968867 | pubmed:author | pubmed-author:SchwartzB RBR | lld:pubmed |
| pubmed-article:3968867 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:3968867 | pubmed:volume | 52 | lld:pubmed |
| pubmed-article:3968867 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:3968867 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:3968867 | pubmed:pagination | 141-50 | lld:pubmed |
| pubmed-article:3968867 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:3968867 | pubmed:year | 1985 | lld:pubmed |
| pubmed-article:3968867 | pubmed:articleTitle | Activated neutrophils disrupt endothelial monolayer integrity by an oxygen radical-independent mechanism. | lld:pubmed |
| pubmed-article:3968867 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:3968867 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:3968867 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:3968867 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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