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Alterations in human leukocyte function induced by ingestion of eicosapentaenoic acid

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Abstract

Two groups of six adults with persistent asthma, who were identical clinically, received 0.1 or 4 g of purified eicosapentaenoic acid ethyl ester (EPA) daily for 8 weeks. Both doses increased significantly the generation of leukotriene B5 (LTB5) from EPA by polymorphonuclear (PMN) and mononuclear leukocytes, while only the high dose decreased leukocyte arachidonic acid (AA) and the generation of LTB4 and prostaglandin E2 from AA. Only the high dose led to inhibition of PMN leukocyte chemotaxis to multiple stimuli by a mean of 57–70% (P<0.01), without altering monocyte chemotaxis, the production of plateletactivating factor by mononuclear leukocytes, or the IgE-dependent release of histamine from basophils. Both doses of EPA increased the responses of T lymphocytes to phytohemagglutinin by a mean of 73% or more (P<0.01) without modifying the numbers of helper and suppressor T lymphocytes. EPA affects the functions of several types of leukocytes critical to inflammation and immunity.

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Authors and Affiliations

  1. Howard Hughes Medical Institute, University of California Medical Center, 94143-0724, San Francisco, California

    Donald G. Payan, Tania Chernov-Rogan & Edward J. Goetzl

  2. Department of Medicine, University of California Medical Center, 94143-0724, San Francisco, California

    Donald G. Payan, Michael Y. S. Wong, Tania Chernov-Rogan, Frank H. Valone, Warren M. Gold & Edward J. Goetzl

  3. School of Pharmacy, University of California Medical Center, 94143-0914, San Francisco, California

    Vincent A. Blake

  4. Lederle Laboratories, 10965, Pearl River, New York

    Walter C. Pickett

Authors
  1. Donald G. Payan
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  2. Michael Y. S. Wong
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  3. Tania Chernov-Rogan
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  4. Frank H. Valone
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  5. Walter C. Pickett
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  6. Vincent A. Blake
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  7. Warren M. Gold
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  8. Edward J. Goetzl
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Payan, D.G., Wong, M.Y.S., Chernov-Rogan, T. et al. Alterations in human leukocyte function induced by ingestion of eicosapentaenoic acid. J Clin Immunol 6, 402–410 (1986). https://doi.org/10.1007/BF00915380

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  • DOI: https://doi.org/10.1007/BF00915380

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