Non‐classical monocytes frequency and serum vitamin D₃ levels are linked to diabetic foot ulcer associated with peripheral artery disease

Abstract

Aims/IntroductionPeripheral artery disease (PAD) serves as a risk factor for diabetic foot ulcers (DFUs). PAD pathology involves atherosclerosis and impaired immunity. Non‐classical monocytes are believed to have an anti‐inflammatory role. 1,25‐Dihydroxy vitamin D (vitamin D3) is claimed to have immune‐modulating and lipid‐regulating roles. Vitamin D receptor is expressed on monocytes. We aimed to investigate if circulating non‐classical monocytes and vitamin D3 were implicated in DFUs associated with PAD.Materials and MethodsThere were two groups of DFU patients: group 1 (n = 40) included patients with first‐degree DFUs not associated with PAD, and group 2 (n = 50) included patients with DFU with PAD. The monocyte phenotypes were detected using flow cytometry. Vitamin D3 was assessed by enzyme‐linked immunosorbent assay.ResultsDFU patients with PAD showed a significant reduction in the frequency of non‐classical monocytes and vitamin D3 levels, when compared with DFU patients without PAD. The percentage of non‐classical monocytes positively correlated with vitamin D3 level (r = 0.4, P < 0.01) and high‐density lipoprotein (r = 0.5, P < 0.001), whereas it was negatively correlated with cholesterol (r = −0.5, P < 0.001). Vitamin D3 was negatively correlated with triglyceride/high‐density lipoprotein (r = −0.4, P < 0.01). Regression analysis showed that a high vitamin D3 serum level was a protective factor against PAD occurrence.ConclusionsNon‐classical monocytes frequency and vitamin D3 levels were significantly reduced in DFU patients with PAD. Non‐classical monocytes frequency was associated with vitamin D3 in DFUs patients, and both parameters were linked to lipid profile. Vitamin D3 upregulation was a risk‐reducing factor for PAD occurrence.

Overview of multifunctional Tregs in cardiovascular disease: From insights into cellular functions to clinical implications

“…Amygdalin, also known as vitamin B17, induces Tregs expansion and upregulates the expression of IL‐10 and TGF‐β in ApoE −/− mice 216 . Orally administered vitamin D3 protects against atherosclerosis by increasing Tregs numbers, promoting tolerogenic DCs, increasing IL‐10 expression, and decreasing IL‐12 expression 217,218 . Therefore, the manipulation of Tregs numbers and immunosuppressive functions through pharmacological approaches (Table 3) may be a promising therapeutic tool for treating atherosclerotic diseases.…”