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Published on: April 16, 2019
PGE2-treated macrophages inhibit development of allergic lung inflammation in mice
Christina Draijer1, Carian E Boorsma1, Catharina Reker-Smit2
1Department of Pharmacokinetics, Toxicology, and Targeting, Groningen Research Institute for Pharmacy, University of Groningen, The Netherlands and Groningen Research Institute for Asthma and COPD, University Medical Center Groningen, University of Groningen, The Netherlands.
Abstract:
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.
Insights
Prostaglandin E2 (PGE2) can restore the balance of immune cells in the lungs, reducing allergic inflammation caused by house dust mites. This approach offers a new therapeutic strategy for asthma and other lung conditions.
Area of Science:
- Immunology
- Pulmonary Medicine
- Inflammation Research
Background:
- Macrophages play a key role in lung inflammation, with their polarization (M1/M2) influencing disease severity.
- Asthma is characterized by a shift in macrophage polarization, favoring pro-inflammatory phenotypes.
- Interleukin-10 (IL-10) producing macrophages are associated with reduced inflammation.
Purpose of the Study:
- To investigate if restoring IL-10 production in macrophages can prevent house dust mite-induced allergic lung inflammation.
- To evaluate the efficacy of Prostaglandin E2 (PGE2) in modulating macrophage polarization and mitigating allergic responses.
Main Methods:
- In vitro assessment of PGE2 as an inducer of IL-10 in macrophages.
- In vivo studies involving house dust mite sensitization and challenge in mice treated with PGE2.
- Evaluation of lung inflammation markers, including eosinophil infiltration and serum YM1 levels.
- Adoptive transfer experiments using PGE2-treated macrophages.
Main Results:
- PGE2 effectively induced IL-10 production in macrophages in vitro.
- Mice treated with free PGE2 exhibited reduced eosinophil infiltration and lower serum YM1 levels compared to controls.
- Adoptive transfer of PGE2-treated macrophages significantly decreased the infiltration of eosinophils, macrophages, CD4+ T cells, and regulatory T cells in the lungs.
Conclusions:
- Repolarization of macrophages towards an IL-10 producing phenotype using PGE2 effectively inhibits the development of allergic lung inflammation.
- Modulating macrophage polarization represents a promising novel therapeutic strategy for allergic lung diseases.
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