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PPARgamma activation primes human monocytes into alternative M2 macrophages with anti-inflammatory properties
M Amine Bouhlel1, Bruno Derudas, Elena Rigamonti
1Institut Pasteur de Lille, F-59019 Lille, France; Inserm, U545, F-59019 Lille, France.
Abstract:
Th1 cytokines promote monocyte differentiation into proatherogenic M1 macrophages, while Th2 cytokines lead to an "alternative" anti-inflammatory M2 macrophage phenotype. Here we show that in human atherosclerotic lesions, the expression of M2 markers and PPARgamma, a nuclear receptor controlling macrophage inflammation, correlate positively. Moreover, PPARgamma activation primes primary human monocytes into M2 differentiation, resulting in a more pronounced anti-inflammatory activity in M1 macrophages. However, PPARgamma activation does not influence M2 marker expression in resting or M1 macrophages, nor does PPARgamma agonist treatment influence the expression of M2 markers in atherosclerotic lesions, indicating that only native monocytes can be primed by PPARgamma activation to an enhanced M2 phenotype. Furthermore, PPARgamma activation significantly increases expression of the M2 marker MR in circulating peripheral blood mononuclear cells. These data demonstrate that PPARgamma activation skews human monocytes toward an anti-inflammatory M2 phenotype.
Insights
Peroxisome proliferator-activated receptor gamma (PPARγ) activation shifts human monocytes toward an anti-inflammatory M2 macrophage phenotype. This priming effect is specific to native monocytes, enhancing their anti-inflammatory capabilities.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- T-helper 1 (Th1) cytokines drive pro-atherogenic M1 macrophage differentiation.
- T-helper 2 (Th2) cytokines promote anti-inflammatory M2 macrophage phenotypes.
- Peroxisome proliferator-activated receptor gamma (PPARγ) is a nuclear receptor regulating macrophage inflammation.
Purpose of the Study:
- To investigate the role of PPARγ in modulating human monocyte differentiation and macrophage phenotype.
- To determine if PPARγ activation influences M2 marker expression in atherosclerotic lesions and circulating cells.
Main Methods:
- Correlation analysis of M2 markers and PPARγ expression in human atherosclerotic lesions.
- In vitro priming of primary human monocytes with PPARγ agonists.
- Assessment of M2 marker expression in resting, M1, and M2 macrophages.
- Analysis of M2 marker MR expression in peripheral blood mononuclear cells.
Main Results:
- Positive correlation observed between M2 markers and PPARγ expression in human atherosclerotic lesions.
- PPARγ activation primes monocytes towards M2 differentiation, enhancing anti-inflammatory activity.
- PPARγ activation does not affect M2 marker expression in resting or M1 macrophages.
- PPARγ agonist treatment does not alter M2 marker expression in atherosclerotic lesions.
- PPARγ activation significantly increases M2 marker MR expression in circulating mononuclear cells.
Conclusions:
- PPARγ activation specifically primes native human monocytes towards an anti-inflammatory M2 phenotype.
- This PPARγ-mediated skewing of monocytes may have therapeutic implications for inflammatory diseases like atherosclerosis.
