Institute for Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany.
German Center for Infection Research (DZIF), Partner Site Bonn-Cologne, Bonn, Germany.
Front Endocrinol (Lausanne). 2020 Apr 28;11:257. doi: 10.3389/fendo.2020.00257. eCollection 2020.
Even after successful weight reduction, obese adults tend to quickly regain the lost weight. This raises the question of whether weight loss improves the underlying chronic adipose tissue inflammation characteristic of obesity. In order to improve our understanding of the mechanisms that reshape metabolic organs during weight loss, we investigated the macrophage and T cell function of the liver and adipose tissue on reversing high fat diet (HFD) mice to normal control diet (NCD). Obese mice that were switched to NCD showed an improvement in their metabolic profile that included enhanced glucose and insulin tolerance, decreased cholesterol, triglyceride, serum glutamic-oxaloacetic transaminase (SGOT), and serum glutamic pyruvic transaminase (SGPT) levels that were comparable to NCD controls. However, despite weight loss, increased frequencies, but not total numbers, of IL-17+ and IL-22+ CD4+ T cells, IFN-γ+ and TNF+ CD8+ T cells and IL-17+ and IL-22+ CD8+ T cells were observed in the adipose tissue of mice switched from HFD to NCD compared to NCD and even HFD fed mice. Further, in the liver, IFN-γ+ and TNF+ CD8+ T cell, IL-17+ and IL-22+ CD8+ T cell, macrophage frequencies and their expression of antigen presenting molecules were increased. To determine if macrophages are the major determinants of the sustained inflammation observed during weight loss, we depleted macrophages, which significantly reduced IFN-γ+, TNF+, IL-17+, and IL-22+ CD8+ T cell frequencies in the liver and the adipose tissue. In conclusion, we show that although weight loss improves the metabolic profile, there is an active and ongoing CD8+ T cell inflammation in liver and adipose tissue mediated by macrophages.
即使在成功减肥后,肥胖成年人往往也会迅速恢复体重。这就提出了一个问题,即减肥是否能改善肥胖症特有的慢性脂肪组织炎症。为了深入了解减肥过程中重塑代谢器官的机制,我们研究了高脂肪饮食(HFD)向正常对照饮食(NCD)转换对肥胖小鼠肝脏和脂肪组织中巨噬细胞和 T 细胞功能的影响。切换到 NCD 的肥胖小鼠的代谢特征得到了改善,包括增强葡萄糖和胰岛素耐量、降低胆固醇、甘油三酯、血清谷氨酸草酰乙酸转氨酶(SGOT)和血清谷氨酸丙酮酸转氨酶(SGPT)水平,这些水平与 NCD 对照相当。然而,尽管体重减轻,但与 NCD 对照甚至 HFD 喂养的小鼠相比,从 HFD 切换到 NCD 的小鼠脂肪组织中观察到 IL-17+和 IL-22+CD4+T 细胞、IFN-γ+和 TNF+CD8+T 细胞以及 IL-17+和 IL-22+CD8+T 细胞的频率增加,而不是总数增加。此外,在肝脏中,IFN-γ+和 TNF+CD8+T 细胞、IL-17+和 IL-22+CD8+T 细胞、巨噬细胞频率及其抗原呈递分子的表达均增加。为了确定巨噬细胞是否是减肥过程中持续炎症的主要决定因素,我们耗尽了巨噬细胞,这显著降低了肝脏和脂肪组织中 IFN-γ+、TNF+、IL-17+和 IL-22+CD8+T 细胞的频率。总之,我们表明,尽管减肥可以改善代谢特征,但在肝脏和脂肪组织中仍存在由巨噬细胞介导的持续的 CD8+T 细胞炎症。