Abstract
It has been shown that vitamin D deficiency increases an individual’s susceptibility to tuberculosis (TB). However, very little is known about the effect of vitamin D on the immune response to Mycobacterium tuberculosis (M. tb) in dendritic cells (DCs). Because DCs play an important role in TB infection, we investigated the phenotypic characteristics and functional capabilities of mouse bone marrow-derived dendritic cells (BMDCs) after stimulation with Bacillus Calmette-Guérin (BCG) in the presence or absence of 25(OH)D3(100 nM). Bone marrow cells from mice were cultured with GM-CSF (20 ng/ml) and were then treated with 25(OH)D3 for 7 days. On day 6, 5 µg/ml of BCG (≥1.0×106 CFU/mg) was added to the cells for 24 hours, and on day 7, the non-adherent cells were harvested for phenotypic and functional analyses. After incubation with 25(OH)D3, the expression levels of MHC-II and CD86 on the surface of the dendritic cells (DCs) and the ability of the DCs to stimulate proliferation of allogeneic mixed lymphocytes were lower than control cells (p<0.05). Furthermore, the level of Interleukin (IL) -4 secreted by the BMDCs in the 25(OH)D3 culture was lower than that in the control culture (p<0.01). However, the BMDCs cultured with 25(OH)D3 produced significantly higher levels of IL-2, IL-6, IL-10 and interferon gamma(IFN-γ) than those in the control culture (p<0.05). These findings suggest that 25(OH)D3 modulates the immune response during mycobacterial infection by affecting the maturation and function of DCs.
Highlights
Tuberculosis (TB) is a major global disease that is estimated to kill 1.45 million people in 2010 [1]
Vitamin D Metabolites Inhibit dendritic cells (DCs) Maturation The BM cultures were pulsed on day 6 with 5 mg/ml of Bacillus Calmette-Guerin (BCG) for 24 h
Vitamin D deficiency is associated with an increased risk of tuberculosis in various populations [22,23]
Summary
Tuberculosis (TB) is a major global disease that is estimated to kill 1.45 million people in 2010 [1]. Calciferol (Vitamin D) was used to treat tuberculosis in the late 1940s and treatment was rationalised based on its role in the calcification of tuberculosis lesions. With the advent of effective anti-tuberculosis drugs in the mid-1950s, the enthusiasm for treating tuberculosis with vitamin D subsided [2]. Increasingly more patients with tuberculosis are infected with drug-resistant strains [3,4], the infection is harder to treat as normal treatment regimes are ineffective. Nursyam et al [6] reported that there were more TB patients with radiological improvement in the vitamin D group. Wejse et al [8] stated that vitamin D does not improve clinical outcome among patients with TB and the trial showed no overall effect on mortality in patients with TB. More detailed studies are necessary to further elucidate the role of vitamin D in TB infection
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