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Adriamycin promotes macrophage dysfunction in mice.

Reto Asmis1, Mu Qiao, Randall R Rossi

  • 1Division of Nephrology, University of Texas Health Science Center at San Antonio and South Texas Veterans Health Care System, 7703 Floyd Curl Drive, MSC 7882, San Antonio, TX 78229, USA. asmis@uthscsa.edu

Free Radical Biology & Medicine
|June 20, 2006
PubMed
Summary
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Adriamycin chemotherapy impairs wound healing by causing oxidative stress and macrophage dysfunction. This study shows low adriamycin doses reduce macrophage numbers and function, delaying tissue repair in mice.

Area of Science:

  • Immunology
  • Cell Biology
  • Oncology

Background:

  • Impaired wound healing is a significant complication of adriamycin chemotherapy.
  • Macrophages are critical for tissue repair, and their dysfunction can impede healing.
  • Previous research indicated adriamycin induces oxidative stress in cultured macrophages.

Purpose of the Study:

  • To investigate if adriamycin induces oxidative stress and macrophage dysfunction in vivo.
  • To determine the effect of adriamycin on wound healing in a mouse model.
  • To explore the link between adriamycin-induced macrophage dysfunction and delayed tissue repair.

Main Methods:

  • FVB mice received low-dose adriamycin or saline injections twice weekly for 8 weeks.
  • Wound healing was assessed in treated and control mice.

Related Experiment Videos

  • Macrophage populations, recruitment, cytokine secretion (TNF-alpha, IL-1beta), reactive oxygen species (ROS) formation, and protein-S-glutathionylation were analyzed.

    • Main Results:

    • Adriamycin treatment significantly delayed wound healing.
    • A decrease in resident peritoneal macrophages and impaired macrophage recruitment was observed.
    • Adriamycin-treated mice showed reduced LPS-induced TNF-alpha and IL-1beta secretion.
    • Macrophages from adriamycin-treated mice exhibited increased ROS production and protein-S-glutathionylation.

    Conclusions:

    • Low cumulative doses of adriamycin induce sustained thiol oxidative stress and macrophage dysfunction in vivo.
    • Adriamycin-impaired macrophage function contributes to delayed tissue repair.
    • Targeting macrophage dysfunction may improve wound healing in patients undergoing adriamycin chemotherapy.