ArticleThe Journal of clinical investigation1994
Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.
Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
The trial behind it
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
23 citing papers in PubMed, 81 citations in OpenAlex.
- Extracorporeal Photopheresis: Secreted Factors That Promote Immunomodulation.Transplantation direct · 2025Article
- Bovine neutrophil migration, CD11a/CD18 expression, and cytokine response to co-culture with mammary gland endothelial cells and epithelial cells.Journal of animal science · 2025Article
- 15-Lipoxygenase promotes resolution of inflammation in lymphedema by controlling TNature communications · 2024Article
- Development of Adaptive Immunity and Its Role in Lung Remodeling.Advances in experimental medicine and biology · 2023Article
- Eicosanoids in inflammation in the blood and the vessel.Frontiers in pharmacology · 2022Review
- Anti-allergic Hydroxy Fatty Acids fromFrontiers in pharmacology · 2017Article
- 15-Lipoxygenases regulate the production of chemokines in human lung macrophages.British journal of pharmacology · 2015Article
- 12/15-Lipoxygenase metabolites of arachidonic acid activate PPARγ: a possible neuroprotective effect in ischemic brain.Journal of lipid research · 2015Article
- Gamma linolenic acid exerts anti-inflammatory and anti-fibrotic effects in diabetic nephropathy.Yonsei medical journal · 2012Article
- Eliminating or blocking 12/15-lipoxygenase reduces neutrophil recruitment in mouse models of acute lung injury.Critical care (London, England) · 2012Article
- PPARs and lipid ligands in inflammation and metabolism.Chemical reviews · 2011Article
- Leukotriene b4 and its metabolites prime the neutrophil oxidase and induce proinflammatory activation of human pulmonary microvascular endothelial cells.Shock (Augusta, Ga.) · 2011Article
- Functional and pathological roles of the 12- and 15-lipoxygenases.Progress in lipid research · 2011Review
- Hematopoietic stem cell function requires 12/15-lipoxygenase-dependent fatty acid metabolism.Blood · 2010Article
- Improved survival and reduced vascular permeability by eliminating or blocking 12/15-lipoxygenase in mouse models of acute lung injury (ALI).Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Article
- Apoptotic human cells inhibit migration of granulocytes via release of lactoferrin.The Journal of clinical investigation · 2009Article
- Transfection of rat kidney with human 15-lipoxygenase suppresses inflammation and preserves function in experimental glomerulonephritis.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- Apoptosis of endothelial cells is associated with paracrine induction of adhesion molecules: evidence for an interleukin-1beta-dependent paracrine loop.The American journal of pathology · 1998Article
- Altered responses of human macrophages to lipopolysaccharide by hydroperoxy eicosatetraenoic acid, hydroxy eicosatetraenoic acid, and arachidonic acid. Inhibition of tumor necrosis factor production.The Journal of clinical investigation · 1997Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
5-Lipoxygenase products, such as leukotrienes, are important stimuli for leukocyte-mediated tissue injury in acute inflammation. 15-Hydroxyeicosatetraenoic acid (15-HETE) is an eicosanoid generated by a variety of cell types via the actions of 15-lipoxygenases and, in addition, cyclooxygenases and epoxygenases. 15-HETE levels are frequently elevated at sites of inflammation, and extracellular 15(S)-HETE is esterified rapidly into neutrophil (PMN) phospholipids in vitro to levels that are comparable with arachidonic acid. We present evidence that remodeling of PMN phospholipids with 15(S)-HETE stereoselectively inhibits PMN migration across endothelium in response to leukotriene B4 (LTB4) and other chemoattractants. Esterified 15(S)-HETE causes a striking reduction in the affinity of LTB4 cell-surface receptors for their ligand and inhibition of LTB4-triggered stimulus-response coupling. As a result of these actions, esterified 15(S)-HETE attenuates the cytoskeletal rearrangements and CD11/CD18-mediated adhesive events that subserve directed locomotion of PMN across endothelium. These observations indicate that products of the 5-lipoxygenase and 15-lipoxygenase pathways can exert counterbalancing influences on PMN trafficking across endothelium. They suggest that 15(S)-HETE may be a potent endogenous inhibitor of PMN-endothelial interactions in vivo and serve to limit or reverse acute inflammation.
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