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Human Macrophages May Normally be “Primed” for a Strong Oxygen Radical Response

  • Michael J. Pabst
  • Nancy P. Cummings
  • Holly B. Hedegaard
  • Richard B. JohnstonJr.
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 166)

Abstract

In previous work we showed that macrophages must produce oxygen radicals in order to kill pathogenic organisms (1). Oxygen radical production by mouse peritoneal macrophages could be enhanced at least ten-fold if the macrophages were previously “activated”. (Throughout this paper we use the term “activated” to mean “primed to release optimal amounts of O 2 when stimulated”). Macrophages were activated either by infecting the animals with Mycobacterium bovis, strain BCG, or by injecting them with bacterial lipopolysaccharide (LPS) or muramyl dipeptide (MDP) (2, 3). Cultured macrophages could also be activated in vitro by addition of LPS or MDP to the cultures (4). Treatment with LPS or MDP enhanced the ability of cultured macrophages to kill bacteria and fungi in vitro (1, 3). Treatment of mice with MDP in vivo enabled them to resist an otherwise lethal challenge infection with Klebsiella pneumoniae or Candida albicans (3, 5).

Keywords

Peritoneal Macrophage Phorbol Myristate Acetate Human Macrophage Phorbol Myristate Acetate Mouse Peritoneal Macrophage 
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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References

  1. 1.
    Sasada, M., and R. B. Johnston, Jr. 1980. Macrophage microbicidal activity. Correlation between phagocytosis-associated oxidative metabolism and the killing of Candida by macrophages. J. Exp. Med. 152: 85.PubMedCrossRefGoogle Scholar
  2. 2.
    Johnston, R. B., Jr., C. A. Godzik and Z. A. Cohn. 1978. Increased superoxide anion production by immunologically activated and chemically elicited macrophages. J. Exp. Med. 148: 115.PubMedCrossRefGoogle Scholar
  3. 3.
    Cummings, N. P., M. J. Pabst and R. B. Johnston, Jr. 1980. Activation of macrophages for enhanced release of superoxide anion and greater killing of Candida albicans by injection of muramyl dipeptide. J. Exp. Med. 152: 1659.PubMedCrossRefGoogle Scholar
  4. 4.
    Pabst, M. J. and R. B. Johnston, Jr. 1980. Increased production of superoxide anion by macrophages exposed in vitro to muramyl dipeptide or lipopolysaccharide. J. Exp. Med. 151: 101.PubMedCrossRefGoogle Scholar
  5. 5.
    Chedid, L., M. Parant, F. Parant, F. Audibert, F. LeFrancier, J. Choay, and M. Sela. 1979. Enhancement of certain biological activities of muramyl dipeptide derivatives after conjugation to a multi-poly (DL-alanine)-poly(L-lysine) carrier. Proc. Natl. Acad. Sci. 76: 6557.PubMedCrossRefGoogle Scholar
  6. 6.
    Pabst, M. J., H. B. Hedesgaard, and R. B. Johnston, Jr. 1982. Cultured human monocytes require exposure to bacterial products to maintain an optimal oxygen radical response. J. Immunol. 128: 123.PubMedGoogle Scholar
  7. 7.
    Hedegaard, H. B., and M. J. Pabst. 1982. Preservation of superoxide anion-generating capacity in cultured human monocytes by treatment with muramyl dipeptide or lipopolysaccharide, p. 205 208. Y. Yamamura et al (eds.), In Immunomodulation by Microbial Products and Related Synthetic Compounds. Excerpta Medica, Amsterdam.Google Scholar

Copyright information

© Springer Science+Business Media New York 1983

Authors and Affiliations

  • Michael J. Pabst
    • 1
  • Nancy P. Cummings
    • 1
  • Holly B. Hedegaard
    • 1
  • Richard B. JohnstonJr.
    • 1
  1. 1.Department of Pediatrics and University of Colorado School of Medicine, Departments of Biochemistry and PediatricsNational Jewish Hospital and Research Center/National Asthma CenterDenverUSA

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