Abstract
Low-grade inflammation plays significant role in the development of diabetes mellitus type 2 (DM2) and impaired glucose tolerance (IGT), but immune regulatory mechanisms involved in these processes are studied incompletely. The purpose of the present study was to characterize the subsets of T-helper-1 (Th1), Th17 and T-regulatory lymphocytes (Treg) in hypertensive patients with DM2 or IGT according to the clinical variant of the disease. Hypertensive patients with DM2 (n = 20) and IGT (n = 7) were recruited in the study. Hypertensive patients without carbohydrate disturbances (n = 7) and healthy volunteers (n = 12) constituted comparison groups. All patients underwent thorough clinical examination. Th1-, Th17- and Th1/Th17-lymphocytes were assessed in peripheral blood mononuclear cells (PBMC) according to intracellular production of interferon (IFN)-γ and interleukin (IL)-17. Expression of receptor to IL-23 (IL-23R) by PBMC was evaluated. Treg-lymphocytes were detected in PBMC by expression of transcription factor FoxP3. Cells were analyzed using flow cytometry. We found that ratio Treg/Th17 was lower and numbers of IL-23R-positive cells were higher in hypertensive patients with IGT. Patients with DM2 were characterized by elevated numbers of Th17-lymphocytes in intact PBMC culture and Th1-lymphocytes after PBMC activation, as well as decreased ratios Treg/Th17 and Treg/Th1, and reduced numbers of Tregs that were inversely related to visceral adiposity index. In hypertensive patients with DM2 glomerular filtration rate was related to numbers of intact Th17- and IL-23R+ cells and FoxP3+ Treg-lymphocytes, while values of Treg/Th1 ratio were interconnected with visceral adiposity index and concentrations of total cholesterol and LDL-cholesterol. Our study underlines the importance of immune imbalance in the development of carbohydrate metabolism perturbations in hypertensive patients even at the stage of impaired glucose tolerance. Further prospective research is needed to elaborate the possible strategy of the risk evaluation for hypertensive DM2 and IGT patients according to their current inflammatory status and propose therapeutic approaches for its correction.
Highlights
Low-grade inflammation plays significant role in the development of diabetes mellitus type 2 (DM2) and impaired glucose tolerance (IGT), but immune regulatory mechanisms involved in these processes are studied incompletely
Analysis of Th1, T-helper lymphocytes type 17 (Th17) and Th1/Th17 lymphocytes showed that patients with DM2 had elevated numbers of Th17 in intact peripheral blood mononuclear cells (PBMC) culture, elevated numbers of Th1 after stimulation of PBMC with PMA + ionomycin and lowered numbers of Th1/Th17 double-positive lymphocytes compared to healthy volunteers (Fig. 1)
Th1/Th17-cells of IGT patients were characterized by lower MFI of IL-17 in intact CD4+ lymphocytes compared to patients with arterial hypertension (AH) (p = 0.018), with DM2 (p = 0.001) and healthy volunteers (p = 0.008) (Table 2)
Summary
Low-grade inflammation plays significant role in the development of diabetes mellitus type 2 (DM2) and impaired glucose tolerance (IGT), but immune regulatory mechanisms involved in these processes are studied incompletely. The purpose of the present study was to characterize the subsets of T-helper-1 (Th1), Th17 and T-regulatory lymphocytes (Treg) in hypertensive patients with DM2 or IGT according to the clinical variant of the disease. The presence of diabetes mellitus type 2 (DM2) in patients with arterial hypertension (AH) significantly amplifies development of microvascular and macrovascular complications, and results in increased mortality [1, 2]. IGT precedes the development of DM2 in 25 % of cases, and patients with IGT have high risk of vascular complications [3, 7]
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