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脂肪来源干细胞促进巨噬细胞从M1型向M2型极化

[Adipose-derived stem cells promote the polarization from M1 macrophages to M2 macrophages].

作者信息

Yin Xuehong, Pang Chunyan, Bai Li, Zhang Ying, Geng Lixia

机构信息

First Affiliated Hospital, Baotou Medical College, Baotou 014040, China.

First Affiliated Hospital, Baotou Medical College, Baotou 014040, China. *Corresponding author, E-mail:

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2016 Mar;32(3):332-8.

Abstract

OBJECTIVE

To investigate the effects of adipose-derived stem cells (ADSCs) on M1/M2 macrophages and whether ADSCs are able to promote the polarization from M1 macrophages to M2 macrophages.

METHODS

M1 macrophages were induced from J774.1 macrophages by 24-hour stimulation of lipopolysaccharide (LPS) and interferon γ (IFN-γ), and M2 macrophages were induced from J774.1 macrophages by interleukin 4 (IL-4) for another 24 hours. Then M1/M2 macrophages were separately cultured in the presence of ADSCs for 24 hours. The M1/M2 macrophages and their corresponding supernatants were collected for further analysis. The expressions of IL-6, tumor necrosis factor α (TNF-α), inducible nitric oxide synthase (iNOS), CC chemokine ligand 2 (CCL2), CD86, arginase 1 (Arg1), mannose receptors/CD206 (MR/CD206), IL-10, found in inflammatory zone 1 (FIZZ1), chitinase 3-like 3 (Ym-1) were detected by real-time PCR and ELISA.

RESULTS

ADSCs significantly decreased the levels of IL-6, TNF-α, iNOS, CCL2 and CD86, and increased the levels of Arg1, CD206 and IL-10 in M1 macrophages. In the supernatant of M1 macrophages, the expressions of IL-6 and TNF-α were reduced, while those of CD206 were enhanced. In M2 macrophages, ADSCs resulted in down-regulation of IL-6, TNF-α, iNOS, CD86 and up-regulation of Arg1, CD206, FIZZ-1, Ym-1 and IL-10. In the supernatant of M2 macrophages, the expression levels of IL-6 and TNF-α were down-regulated and those of CD206 were up-regulated.

CONCLUSION

ADSCs can inhibit the gene expression of M1 macrophages and promote the gene expression of M2 macrophages, as well as mediate the polarization from M1 macrophages to M2 macrophages.

摘要

目的

研究脂肪来源干细胞(ADSCs)对M1/M2巨噬细胞的影响,以及ADSCs是否能够促进M1巨噬细胞向M2巨噬细胞极化。

方法

通过脂多糖(LPS)和干扰素γ(IFN-γ)刺激24小时从J774.1巨噬细胞诱导出M1巨噬细胞,通过白细胞介素4(IL-4)再刺激24小时从J774.1巨噬细胞诱导出M2巨噬细胞。然后将M1/M2巨噬细胞分别与ADSCs共同培养24小时。收集M1/M2巨噬细胞及其相应的上清液用于进一步分析。通过实时PCR和ELISA检测炎症区1(FIZZ1)、几丁质酶3样3(Ym-1)中白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)、诱导型一氧化氮合酶(iNOS)、CC趋化因子配体2(CCL2)、CD86、精氨酸酶1(Arg1)、甘露糖受体/CD206(MR/CD206)、IL-10的表达。

结果

ADSCs显著降低M1巨噬细胞中IL-6、TNF-α、iNOS、CCL2和CD86的水平,并增加Arg1、CD206和IL-10的水平。在M1巨噬细胞的上清液中,IL-6和TNF-α的表达降低,而CD206的表达增强。在M2巨噬细胞中,ADSCs导致IL-6、TNF-α、iNOS、CD86下调,Arg1、CD206、FIZZ-1、Ym-1和IL-10上调。在M2巨噬细胞的上清液中,IL-6和TNF-α的表达水平下调,CD206的表达上调。

结论

ADSCs可抑制M1巨噬细胞的基因表达,促进M2巨噬细胞的基因表达,并介导M1巨噬细胞向M2巨噬细胞极化。

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