Isoproterenol inhibition of isolated human neutrophil function

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Abstract

The human PMN can contribute to the inflammatory response. Several neutrophil responses can be inhibited by agonists that increase the cellular levels of cyclic AMP. In the following article, we compared the effects of ISO on lysosomal beta-glucuronidase release, superoxide generation, and CL in isolated human PMNs. ISO inhibited the neutrophil CL response to opsonized zymosan in a dose-dependent fashion with maximal effects at 10−4M. ISO inhibition of CL was not enhanced by the addition of theophylline, nor was CL inhibited by the exogenous addition cyclic AMP except at a very high concentration of 10−3M. ISO also suppressed beta-glucuronidase release and superoxide generation in neutrophils during an incubation with opsonized zymosan particles. For ISO to inhibit beta-glucuronidase release and superoxide generation, theophylline (5 × 10−4M) was necessary. ISO effectively inhibits three neutrophil functions that are capable of causing tissue inflammation. Although ISO suppressed all three neutrophil responses, the inhibitory mechanisms appear to be variable.

References (29)

  • RB Zurier et al.

    Mechanisms of lysosomal enzyme release from human leukocytes. II. Effects of cAMP and cGMP, autonomic agonists, and agents which affect microtubule function

    J Clin Invest

    (1974)
  • WW Busse et al.

    Histamine inhibition of neutrophil lysosomal enzyme release: an H2 histamine receptor response

    Science

    (1976)
  • LR DeChatelet

    Initiation of the respiratory burst in human polymorphonuclear neutrophils: a critical review

    J Reticuloendothel Soc

    (1978)
  • JM McCord et al.

    The biology of oxygen radicals

    Ann Intern Med

    (1978)
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    Supported by a grant from the National Institutes of Health, AI 10404 and AI 15685.

    Dr. Busse is a recipient of an Allergic Disease Academic Award No. AI 00343 from the National Institutes of Health, National Institutes of Allergy and Infectious Disease.

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