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首页> 外文期刊>Progress in Artificial Intelligence >Modification of Tumor Necrosis Factor-alpha and C-C Motif Chemokine Ligand 18 Secretion by Monocytes Derived from Patients with Diabetic Foot Syndrome
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Modification of Tumor Necrosis Factor-alpha and C-C Motif Chemokine Ligand 18 Secretion by Monocytes Derived from Patients with Diabetic Foot Syndrome

机译：糖尿病足综合征患者肿瘤坏死因子-α和C-C基序趋化因子配体18分泌的单核细胞分泌

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Background: This study involves the investigation of spontaneous and induced secretion of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) and the anti-inflammatory chemokine C-C motif chemokine ligand 18 (CCL18) by monocytes isolated from blood of patients with long-term type 2 diabetes mellitus (T2DM), both with or without foot ulcers. Methods: A total of 121 patients with T2DM (79 without diabetic foot syndrome (DFS) and 42 patients with DFS) were included. Cluster of Differentiation 14 (CD14+) monocytes were isolated from patients' blood and stimulated by interferon-gamma (IFN-gamma) and interleukin-4 (IL-4) for induction of pro- and anti-inflammatory monocyte activation, respectively. The concentrations of TNF-alpha and CCL18 in the culture medium were measured using ELISA on day 1 and day 6 after cell stimulation. Results: We found a correlation between glycated hemoglobin (HbA1c) and stimulated secretion levels of TNF-alpha (r = 0.726, p = 0.027) and CCL18 (r = -0.949, p = 0.051) in patients with DFS. There was an increase of pro- and anti-inflammatory activation of monocytes in all patients with different durations of DFS (p < 0.05). However, no stimulation of anti-inflammatory activation was detected in patients with DFS lasting more than 6 months (p = 0.033). Conclusions: Our study showed an increase in pro-inflammatory secretion and a decrease in anti-inflammatory secretion by monocytes isolated from blood of patients with T2DM depending on HbA1c levels and duration of the inflammatory process. These findings allow us to assume that monocytes isolated from T2DM patients are characterized by a biased ability to respond towards pro-inflammatory stimulation, contributing to the chronic wound process.
机译：背景：该研究涉及通过单核细胞分离出从患者血液中分离的单核细胞来调查自发性和诱导的促炎细胞因子肿瘤坏死因子-α（TNF-α）和抗炎趋化因子CC MOTIF趋化因子18（CCL18）的抗炎趋化因子CC趋化因子18（CCL18）长期2型糖尿病（T2DM），无论有或没有足部溃疡。方法：还包括总共121例T2DM患者（没有糖尿病足综合征（DFS）和42例DFS患者）。分化14（CD14 +）单核细胞分离出从患者的血液中分离，并受到干扰素-γ（IFN-Gamma）和白细胞介素-4（IL-4）的刺激，分别用于诱导促炎和抗炎单核细胞活化。在细胞刺激后第1天和第6天使用ELISA测量培养基中TNF-α和CCL18的浓度。结果：我们发现糖化血红蛋白（HBA1C）与DFS患者的TNF-α（R = 0.726，P = 0.027）和CCL18（R = -0.949，P = 0.051）的刺激分泌水平之间的相关性。所有患有不同DFS患者的所有患者的单核细胞有促进和抗炎活化的增加（P <0.05）。然而，在持续超过6个月的DFS患者中检测到对抗炎活化的刺激（P = 0.033）。结论：我们的研究表明，根据HBA1C水平和炎症过程的持续时间，通过T2DM患者分离的单核细胞分离的单核细胞分离的促炎症分泌的增加和抗炎分泌减少。这些发现允许我们假设从T2DM患者中分离的单核细胞的特征在于偏见促进促炎刺激的能力，有助于慢性伤口过程。

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