ArticleProceedings of the National Academy of Sciences of the United States of America1994
Intrinsic 5-lipoxygenase activity is required for neutrophil responsivity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- Not just sugar: metabolic control of neutrophil development and effector functions.Journal of leukocyte biology · 2024Review
- Functional genomic assessment of phosgene-induced acute lung injury in mice.American journal of respiratory cell and molecular biology · 2013Article
- Circulating leukotriene B4 identifies respiratory complications after trauma.Mediators of inflammation · 2012Article
- Leukotriene biosynthesis inhibition ameliorates acute lung injury following hemorrhagic shock in rats.Journal of cardiothoracic surgery · 2011Article
- Article
- Decreased leukotriene release from neutrophils after severe trauma: role of immature cells.Inflammation · 2001Article
- Inhibition of leukotriene formation and IL-8 release by the paf-receptor antagonist SM-12502.Inflammation · 1996Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We found that intrinsic neutrophil 5-lipoxygenase activity was necessary for human neutrophil adherence and chemotaxis in vitro and human neutrophil-mediated acute edematous injury in isolated perfused rat lungs given interleukin 8 intratracheally. Treatment with either Zileuton (a specific reversible competitive inhibitor of 5-lipoxygenase) or MK886 (a specific irreversible inhibitor of the 5-lipoxygenase activator protein) prevented stimulated neutrophil adherence and chemotaxis (but not superoxide anion production) in vitro. Zileuton- or MK886-inhibited neutrophil chemotaxis was not restored by adding leukotriene B4 in vitro. Perfusion with neutrophils and either Zileuton or MK886, or with MK886-pretreated neutrophils (without adding MK886 to the perfusate), also prevented lung injury (reflected by lung weight gain and lung Ficoll retention) and perfusate leukotriene B4 increases in isolated rat lungs given interleukin 8 intratracheally. Again, adding leukotriene B4 to the perfusate did not damage interleukin 8-treated isolated lungs perfused with Zileuton-inhibited neutrophils. We conclude that intrinsic 5-lipoxygenase activity is required for neutrophil adherence and chemotaxis and neutrophil-mediated lung injury.
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Registered trials
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