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Generation and recognition of leukotriene mediators of hypersensitivity and inflammation

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Abstract

The potent mediators generated by the 5- and 15-lipoxygenation of arachidonic acid have diverse effects on smooth muscles, blood vessels, leukocytes, epithelial cells and glands, and sensory neurons, which suggest possible roles in the initiation and regulation of physiological and biochemical events. The responses to leukotrienes and related mediators are attributable to binding by stereospecific cellular receptors and consequent activation of biochemical transductional sequences analogous to those characteristic of other receptor systems. The elevated concentrations of these mediators in lesional fluids and tissues of inflammatory bowel disease and other hypersensitivity and inflammatory states are, in some instances, clearly related to the time course of development of the disease process. Systematic application of specific inhibitors and antagonists that are becoming available will define more clearly the involvement of leukotrienes in health and disease and possibly lead to new therapeutic approaches.

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Authors and Affiliations

  1. Howard Hughes Medical Institute, USA

    Edward J. Goetzl MD, Barbara A. Burrall MD, Laurent Baud MD, Kirsten H. Scriven AB, Jon D. Levine MD, PhD & Catherine H. Koo PhD

  2. Departments of Medicine and Microbiology-Immunology, University of California Medical Center, 94143-0724, San Francisco, California

    Edward J. Goetzl MD, Barbara A. Burrall MD, Laurent Baud MD, Kirsten H. Scriven AB, Jon D. Levine MD, PhD & Catherine H. Koo PhD

Authors
  1. Edward J. Goetzl MD
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  2. Barbara A. Burrall MD
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  3. Laurent Baud MD
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  4. Kirsten H. Scriven AB
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  5. Jon D. Levine MD, PhD
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  6. Catherine H. Koo PhD
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Additional information

Supported in part by grants HL31809 and AI19784 from the National Institutes of Health. Dr. Burrall was supported by Physician Scientist Award K11AI00668 from the NIAID.

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Goetzl, E.J., Burrall, B.A., Baud, L. et al. Generation and recognition of leukotriene mediators of hypersensitivity and inflammation. Digest Dis Sci 33 (Suppl 3), 36S–40S (1988). https://doi.org/10.1007/BF01538129

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