Macrophages are central to inflammatory response and become polarized towards the M1 or M2 states upon activation by immunostimulants. In this study, we investigated the effects of lipopolysaccharides (LPS) and interleukin (IL)-17A on the activation of macrophages in in vivo mouse skin. We examined whether macrophages are activated in the skin of imiquimod (IMQ)-treated mice, a model for IL-17A-induced psoriasis-like skin inflammation, and flaky-tail (Flg ^ft ) mice, a model for IL-17A-induced chronic atopic dermatitis-like skin inflammation. LPS and IL-17A independently increased the expression levels of iNOS, CX3CR1, CD206, phospho-STAT1 and phospho-STAT3 proteins in the skin of B6 mice, and the effects of LPS was not altered by IL-17A. The expression levels of these proteins were increased in the skin of IMQ-treated and Flg ^ft mice. IL-17A neutralization increased the expressions of iNOS and phospho-STAT1 in the IMQ-treated skin, but it decreased the expressions of CD206 and phospho-STAT3 proteins in the skin of Flg ^ft mice, suggesting that macrophages to change from the M2 to the M1 state in the skin of these mice. These results suggest that IL-17A is involved in the activation of macrophages that are in the process of adopting the heterogeneous profiles of both the M1 and M2 states.

中文翻译：

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IL-17A诱导异质巨噬细胞，并且它不会改变脂多糖对小鼠皮肤中巨噬细胞活化的影响。

巨噬细胞是炎症反应的中心，在被免疫刺激剂激活后朝着M1或M2状态极化。在这项研究中，我们调查了脂多糖（LPS）和白介素（IL）-17A对体内小鼠皮肤中巨噬细胞活化的影响。我们检查了经咪喹莫特（IMQ）处理的小鼠皮肤中是否激活了巨噬细胞，该模型是IL-17A诱导的牛皮癣样皮肤炎症和片状尾巴的模型（Flg ^ft）小鼠，这是IL-17A诱导的慢性特应性皮炎样皮肤炎症的模型。LPS和IL-17A独立增加B6小鼠皮肤中iNOS，CX3CR1，CD206，磷酸STAT1和磷酸STAT3蛋白的表达水平，而IL-17A不会改变LPS的作用。这些蛋白质的表达水平在IMQ处理的小鼠和Flg ^ft小鼠的皮肤中增加。IL-17A中和可增加经IMQ处理的皮肤中iNOS和磷酸化STAT1的表达，但会降低Flg ^ft皮肤中CD206和磷酸化STAT3蛋白的表达。提示这些小鼠皮肤中巨噬细胞从M2变为M1状态。这些结果表明，IL-17A参与了巨噬细胞的活化，而巨噬细胞的活化则采用了M1和M2状态的异质分布。