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Research Article Free access | 10.1172/JCI116999

Remodeling of neutrophil phospholipids with 15(S)-hydroxyeicosatetraenoic acid inhibits leukotriene B4-induced neutrophil migration across endothelium.

S Takata, M Matsubara, P G Allen, P A Janmey, C N Serhan, and H R Brady

Renal Division, Brigham and Women's Hospital, Boston, Massachusetts.

Find articles by Takata, S. in: PubMed | Google Scholar

Renal Division, Brigham and Women's Hospital, Boston, Massachusetts.

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Renal Division, Brigham and Women's Hospital, Boston, Massachusetts.

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Renal Division, Brigham and Women's Hospital, Boston, Massachusetts.

Find articles by Janmey, P. in: PubMed | Google Scholar

Renal Division, Brigham and Women's Hospital, Boston, Massachusetts.

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Renal Division, Brigham and Women's Hospital, Boston, Massachusetts.

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Published February 1, 1994 - More info

Published in Volume 93, Issue 2 on February 1, 1994
J Clin Invest. 1994;93(2):499–508. https://doi.org/10.1172/JCI116999.
© 1994 The American Society for Clinical Investigation
Published February 1, 1994 - Version history
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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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