PPARγ Activation Primes Human Monocytes into Alternative M2 Macrophages with Anti-inflammatory Properties
2007
Summary 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 PPARγ, a nuclear receptor controlling macrophage inflammation, correlate positively. Moreover, PPARγ activation primes primary human monocytes into M2 differentiation, resulting in a more pronounced anti-inflammatory activity in M1 macrophages. However, PPARγ activation does not influence M2 marker expression in resting or M1 macrophages, nor does PPARγ agonist treatment influence the expression of M2 markers in atherosclerotic lesions, indicating that only native monocytes can be primed by PPARγ activation to an enhanced M2 phenotype. Furthermore, PPARγ activation significantly increases expression of the M2 marker MR in circulating peripheral blood mononuclear cells. These data demonstrate that PPARγ activation skews human monocytes toward an anti-inflammatory M2 phenotype.
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