Besides the classic vitamin D function on bone homeostasis, there are bodies of evidence showing that adequate status of vitamin D can modulate inflammation. We hypothesized that higher plasma levels of 25-hydroxyvitamin D (25[OH]D) would correlate with lower plasma levels of proinflammatory cytokines, acute-phase proteins, and soluble adhesion molecules and higher plasma levels of anti-inflammatory cytokines. We included all adults (age, 20-59 years) of the population-based, cross-sectional study, Health Survey-São Paulo, conducted in São Paulo (Brazil) in the study (n = 281). Anthropometric parameters, blood pressure measurements, and a fasting blood sample were collected by trained fieldworkers. Serum 25(OH)D concentration, plasma inflammatory biomarker levels (C-reactive protein, interleukin [IL]-1β, IL-6, IL-8, IL-10, tumor necrosis factor [TNF] α, IL-12p70, adiponectin, monocyte chemoattractant protein-1, soluble intercellular adhesion molecule-1, and soluble vascular cell adhesion molecule-1), and plasma blood lipid parameters were evaluated. The prevalence of vitamin D inadequacy (<50 nmol/L) was 65.5%. Inadequate participants were younger, with lower body mass index (BMI), systolic and diastolic blood pressures, triglyceride, and total cholesterol levels as well as low-density lipoprotein cholesterol, compared with individuals adequate for vitamin D status. After adjustment, plasma concentration of soluble intercellular adhesion molecule-1 was statistically higher among adequate participants. Stratifying for BMI categories, a negative association was observed between plasma IL-6 and TNF-α levels and serum 25(OH)D concentration in normal-weight participants, whereas a negative association was detected between plasma adiponectin level and serum 25(OH)D concentration in overweight participants. The present findings suggest that BMI interacts with serum 25(OH)D levels, modulating inflammatory response and affecting plasma IL-6, TNF-α, and adiponectin levels. These data indicate that BMI plays a determinant role in the vitamin D-inflammation axis.

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