PGE2-treated macrophages inhibit development of allergic lung inflammation in mice

J Leukoc Biol. 2016 Jul;100(1):95-102. doi: 10.1189/jlb.3MAB1115-505R. Epub 2016 Mar 1.


In healthy lungs, many macrophages are characterized by IL-10 production, and few are characterized by expression of IFN regulatory factor 5 (formerly M1) or YM1 and/or CD206 (formerly M2), whereas in asthma, this balance shifts toward few producing IL-10 and many expressing IFN regulatory factor 5 or YM1/CD206. In this study, we tested whether redressing the balance by reinstating IL-10 production could prevent house dust mite-induced allergic lung inflammation. PGE2 was found to be the best inducer of IL-10 in macrophages in vitro. Mice were then sensitized and challenged to house dust mites during a 2 wk protocol while treated with PGE2 in different ways. Lung inflammation was assessed 3 d after the last house dust mite challenge. House dust mite-exposed mice treated with free PGE2 had fewer infiltrating eosinophils in lungs and lower YM1 serum levels than vehicle-treated mice. Macrophage-specific delivery of PGE2 did not affect lung inflammation. Adoptive transfer of PGE2-treated macrophages led to fewer infiltrating eosinophils, macrophages, (activated) CD4(+), and regulatory T lymphocytes in lungs. Our study shows that the redirection of macrophage polarization by using PGE2 inhibits development of allergic lung inflammation. This beneficial effect of macrophage repolarization is a novel avenue to explore for therapeutic purposes.

Keywords: alveolar; asthma; embryonic; hematopoietic; targeting.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Asthma / etiology
  • Asthma / metabolism
  • Asthma / prevention & control*
  • Cells, Cultured
  • Dinoprostone / metabolism*
  • Eosinophils / cytology
  • Eosinophils / immunology*
  • Female
  • Interleukin-10 / immunology
  • Interleukin-10 / metabolism*
  • Macrophages / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Pneumonia / etiology
  • Pneumonia / metabolism
  • Pneumonia / prevention & control*
  • Pyroglyphidae / pathogenicity*


  • Interleukin-10
  • Dinoprostone