Vitamin D status in coronary artery disease: association with IL-35 and TGF-β1 and disease severity
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Published on: August 9, 2024
Fereshteh Rasa1,2, Nadereh Naderi3,4, Ebrahim Eftekhar5,6
1Department of Biochemistry, College of Science, Fars Science and Research Branch, Islamic Azad University Fars, Iran.
Insights
Vitamin D deficiency is linked to lower levels of TGF-β1 and IL-35 in coronary artery disease (CAD) patients. Vitamin D may protect against atherosclerosis by increasing anti-inflammatory cytokines like TGF-β1.
Area of Science:
- Cardiovascular Research
- Immunology
- Nutritional Science
Background:
- The protective mechanisms of vitamin D against atherosclerosis and coronary heart disease (CAD) are not fully understood.
- Regulatory T cells (Tregs) and their inhibitory cytokines play a role in immune regulation and may be influenced by vitamin D status.
Purpose of the Study:
- To investigate the relationship between vitamin D levels and the concentrations of inhibitory cytokines (TGF-β1 and IL-35) produced by Tregs in patients with CAD.
- To explore the potential role of vitamin D in modulating these cytokines in the context of atherosclerosis severity.
Main Methods:
- 81 CAD patients were categorized into groups based on the number of diseased vessels (none, single, double, triple).
- Serum concentrations of vitamin D, transforming growth factor-beta 1 (TGF-β1), and interleukin-35 (IL-35) were measured using electrochemiluminescence and ELISA assays.
Main Results:
- Patients with no vessel disease had significantly higher vitamin D, TGF-β1, and IL-35 levels compared to those with CAD.
- TGF-β1 and IL-35 levels were positively correlated with vitamin D concentrations and negatively correlated with CAD severity.
- Vitamin D deficiency was associated with significantly lower TGF-β1 levels in CAD patients.
Conclusions:
- Decreased vitamin D levels in CAD patients are associated with lower plasma concentrations of TGF-β1 and IL-35.
- The antiatherosclerotic effects of vitamin D may be partly mediated by its ability to up-regulate anti-inflammatory cytokines, particularly TGF-β1.
- TGF-β1 shows a significant association with vitamin D deficiency in CAD, suggesting a key role in vitamin D's protective effects.
Background:
The exact mechanisms underlying the protective effect of vitamin D in the pathogenesis of atherosclerosis and coronary heart disease are obscure.
Objective:
Here, we have addressed the relation between vitamin D status and regulatory T cells (Tregs) inhibitory cytokines in patients suffering from coronary artery disease (CAD).
Materials And Methods:
81 patients were divided into single (n= 20), double (n=20) and triple (n=20) vessel disease groups and compared to no vessel disease (No VD) group (n=21). Interleukin (IL) -35 and TGF- β1 were measured using ELISA. Vitamin D was measured using Electrochemiluminescence assay.
Results:
Vitamin D, TGF-β1 and IL-35 concentrations in No VD (32.4±15.2, 667.7±427.6, 12.1±11.9 respectively) group were significantly higher than patients with 1 or more vessel disease (18.1±9.8, 360.4±354.1 and 6.8±8.1 respectively, p<0.05). Subgroup analysis revealed that TGF-β1 and IL-35 (but not vitamin D) were significantly higher in double vessel disease patients (591.9±465.7 and 9.2±8.0 respectively) compared to those with triple vessel disease (173.1±163.3 and 3.6±1.4 respectively, p<0.05). Both TGF-β1 and IL-35 were positively correlated to the serum level of vitamin D (r= 0.38, p= 0.001 and r=0.26, p= 0.028 respectively). Vitamin D, TGF-β1 and IL-35 revealed a negative correlation (r= -0.36, r=-0.46 and r-0.024 respectively) with severity of CAD (p< 0.05). Compared to normal serum vitamin D patients (326.6±351.7 pg/mL vs. 754.5±560 pg/mL, p=0.036 respectively) TGF-β1 (but not IL-35), was significantly lower in vitamin D deficient patients.
Conclusion:
The results suggested that, although decreased TGF-β1 and IL-35 plasma levels correlate positively with decreased vitamin D levels and negatively with severity of CAD, but only TGF-β1 has a significant association with vitamin D deficiency in CAD patients. It seems that the antiatherosclerotic effect of vitamin D is at least partly attributed to the up-regulation of anti-inflammatory cytokines especially TGF- β1.
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