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The Respiratory Burst in Activated Macrophages: Studies of Its Molecular Basis and Evidence for Downregulation in Chronic Infection

  • Richard B. JohnstonJr.
  • Seiichi Kitagawa
  • Carl K. EdwardsIII
  • Jacqueline Y. Channon
  • Hitoshi Suzuki
  • Michael J. Pabst
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 239)

Abstract

Macrophages (Kø) elicited by injection of inflammatory agents or obtained from animals infected with intracellular parasites are primed so that they respond to phagocytosis or exposure to phorbol myristate acetate (PMA) with a marked increase in the respiratory burst (1). Unstimulated Mø release little if any reactive oxygen metabolites; stimulation is required to demonstrate the primed state. This capacity for an increased stimulated release of reactive oxygen metabolites appears to play an essential role in the increased microhicidal capacity of activated Mo (2–4). Priming is a manifestation of Mø activation, but it is not the same as activation; i.e., priming may not always reflect the fully activated state (5).

Keywords

NADPH Oxidase Infected Mouse Phosphatidic Acid Respiratory Burst Phorbol Myristate Acetate 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1988

Authors and Affiliations

  • Richard B. JohnstonJr.
    • 1
    • 2
  • Seiichi Kitagawa
    • 1
    • 2
  • Carl K. EdwardsIII
    • 1
    • 2
  • Jacqueline Y. Channon
    • 1
    • 2
  • Hitoshi Suzuki
    • 1
    • 2
  • Michael J. Pabst
    • 1
    • 2
  1. 1.Department of PediatricsUniversity of Pennsylvania School of Medicine and The Children’s Hospital of PhiladelphiaPhiladelphiaUSA
  2. 2.Department of PediatricsNational Jewish Center for Immunology and Respiratory MedicineDenverUSA

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