Abstract
Systemic lupus erythematosus (SLE) is a chronic systemic autoimmune disease that disproportionately affects African American females. The causes of SLE are unknown but postulated to be a combination of genetic predisposition and environmental triggers. Vitamin D deficiency is one of the possible environmental triggers. In this study we evaluated relationships between vitamin D status, cellular aging (telomere length) and anti-telomere antibodies among African American Gullah women with SLE. The study population included African American female SLE patients and unaffected controls from the Sea Island region of South Carolina. Serum 25-hydroxyvitamin D levels were measured using a nonchromatographic radioimmunoassay. Telomere length was measured in genomic DNA of peripheral blood mononuclear cells (PBMCs) by monochrome multiplex quantitative PCR. Anti-telomere antibody levels were measured by enzyme-linked immunosorbent assay (ELISA). Patients with SLE had significantly shorter telomeres and higher anti-telomere antibody titers compared to age- and gender-matched unaffected controls. There was a positive correlation between anti-telomere antibody levels and disease activity among patients and a significant correlation of shorter telomeres with lower 25-hydroxyvitamin D levels in both patients and controls. In follow-up examination of a subset of the patients, the patients who remained vitamin D deficient tended to have shorter telomeres than those patients whose 25-hydroxyvitamin D levels were repleted. Increasing 25-hydroxyvitamin D levels in African American patients with SLE may be beneficial in maintaining telomere length and preventing cellular aging. Moreover, anti-telomere antibody levels may be a promising biomarker of SLE status and disease activity.
Highlights
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with diverse manifestations, with the presence of autoantibodies a unifying feature among patients
[10] Previously, we demonstrated a negative correlation between 25(OH)D and disease activity (SLEDAI score) among an African American Gullah cohort (SLE in Gullah Health or SLEIGH), a correlation which subsequently was demonstrated in many other SLE populations worldwide. [11]
In SLE, vitamin D deficiency is thought to act as a possible trigger of disease and/or disease activity, and cellular aging/ senescence may contribute to disease progression
Summary
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with diverse manifestations, with the presence of autoantibodies a unifying feature among patients. SLE disproportionately affects African Americans and Hispanics with African Americans having higher disease activity, rates of renal involvement, damage accrual and mortality compared to other ethnicities in the United States. Vitamin D deficiency is a potential environmental trigger of SLE and/or SLE-related disease activity. [4] Vitamin D is an essential steroid hormone with well-established effects on mineral metabolism, skeletal health, and more recently described effects on cardiovascular and immune health.[5,6,7] Mounting evidence has revealed that vitamin D deficiency contributes to the morbidity and mortality of multiple chronic diseases. Because patients with SLE avoid the sun, a common trigger of disease flares, the risk of vitamin D deficiency is even higher among SLE patients than in the general population, African Americans with SLE whose dermal pigmentation impedes conversion of vitamin D. Because patients with SLE avoid the sun, a common trigger of disease flares, the risk of vitamin D deficiency is even higher among SLE patients than in the general population, African Americans with SLE whose dermal pigmentation impedes conversion of vitamin D. [4] Vitamin D deficiency was associated with increased antinuclear antibody (ANA) positivity among healthy controls and increased B cell activation among patients with SLE. [10] Previously, we demonstrated a negative correlation between 25(OH)D and disease activity (SLEDAI score) among an African American Gullah cohort (SLE in Gullah Health or SLEIGH), a correlation which subsequently was demonstrated in many other SLE populations worldwide. [11]
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