Analysis of the percentages of monocyte subsets and ILC2s, their relationships with metabolic variables and response to hypocaloric restriction in obesity

Purpose 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 beta 2-adrenergic receptor (beta 2AR) expression in lean and obese subjects, and the possible effect of hypocaloric restriction on these innate immune cells. Methods In 139 individuals aged 45 to 57 years, classified in 74 lean individuals (>18.9kg/m(2) BMI <24.9kg/m(2)) and 65 with obesity (n = 65), we collected fasting blood samples to detect Mo subsets, ILC2s number, and beta 2AR 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. Results Non-classical monocytes (NCM) and beta 2AR 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, beta 2AR expression on IM with REE, but a positive relationship between NCM and HOMA-IR. Caloric restriction allowed a significant diminution of NCM and the beta 2AR expression on IM, as well as, an increase in the percent of classical Mo (CM), and ILC2s. Delta REE was related to Delta CD16(+)/CD16(-) ratio. Conclusions These findings show that in obesity occur changes in NCM, ILC2s and beta 2AR expression, which contribute to the low-grade inflammation linked to obesity and might revert with caloric restriction.