Department of Medical Sciences, University of Guanajuato, León Campus, León, Gto., México.
PLoS One. 2020 Feb 19;15(2):e0228637. doi: 10.1371/journal.pone.0228637. eCollection 2020.
Obesity results from excess energy intake over expenditure and is characterized by chronic low-grade inflammation involving circulating monocytes (Mo) and group 2 innate lymphoid cells (ILC2s) imbalance. We analyzed circulating Mo subsets and ILC2s percentages and β2-adrenergic receptor (β2AR) expression in lean and obese subjects, and the possible effect of hypocaloric restriction on these innate immune cells.
In 139 individuals aged 45 to 57 years, classified in 74 lean individuals (>18.9kg/m2 BMI <24.9kg/m2) and 65 with obesity (n = 65), we collected fasting blood samples to detect Mo subsets, ILC2s number, and β2AR expression by flow cytometry. Lipids, insulin, leptin, and acylated-ghrelin concentrations were quantified. Resting energy expenditure (REE) was estimated by indirect calorimetry. These measurements were repeated in obese subjects after 7-weeks of hypocaloric restriction.
Non-classical monocytes (NCM) and β2AR expression on intermediate Mo (IM) were increased in obese individuals (p<0.001, in both cases), whereas the percent of ILC2s was decreased (p<0.0001). Stepwise regression analysis showed significantly negative associations of ILC2s with caloric intake, β2AR expression on IM with REE, but a positive relationship between NCM and HOMA-IR. Caloric restriction allowed a significant diminution of NCM and the β2AR expression on IM, as well as, an increase in the percent of classical Mo (CM), and ILC2s. ΔREE was related to ΔCD16+/CD16- ratio.
These findings show that in obesity occur changes in NCM, ILC2s and β2AR expression, which contribute to the low-grade inflammation linked to obesity and might revert with caloric restriction.
肥胖是由于能量摄入超过支出而导致的,其特征是循环单核细胞(Mo)和 2 型固有淋巴细胞(ILC2)失衡引起的慢性低度炎症。我们分析了瘦人和肥胖者的循环 Mo 亚群和 ILC2 百分比以及β2 肾上腺素能受体(β2AR)的表达,并研究了低热量限制对这些固有免疫细胞的可能影响。
在 139 名年龄在 45 至 57 岁的个体中,根据 BMI(体重指数)将其分为 74 名瘦人(>18.9kg/m2BMI<24.9kg/m2)和 65 名肥胖者。我们采集空腹血样,通过流式细胞术检测 Mo 亚群、ILC2 数量和β2AR 的表达。定量检测血脂、胰岛素、瘦素和酰化胃饥饿素浓度。通过间接热量测定法估计静息能量消耗(REE)。在肥胖者接受 7 周低热量限制后,重复这些测量。
肥胖个体的非经典单核细胞(NCM)和中间 Mo(IM)上的β2AR 表达增加(均为 p<0.001),而 ILC2 的百分比降低(p<0.0001)。逐步回归分析显示,ILC2s 与热量摄入呈显著负相关,IM 上的β2AR 表达与 REE 呈显著负相关,而 NCM 与 HOMA-IR 呈正相关。热量限制可显著降低 NCM 和 IM 上的β2AR 表达,增加经典 Mo(CM)和 ILC2 的百分比。ΔREE 与 ΔCD16+/CD16- 比值相关。
这些发现表明,肥胖个体中 NCM、ILC2 和β2AR 表达发生变化,这些变化与肥胖相关的低度炎症有关,并且可能随着热量限制而逆转。