BCG stimulation promotes dendritic cell proliferation and expression of VDR and CYP27B1 in vitamin D‑deficient mice.

Vitamin D deficiency may lead to an increased risk of tuberculosis. In the present study, the effects of Mycobacterium tuberculosis (Mtb) infection on dendritic cells (DCs) derived from vitamin D‑deficient mice or normal control mice were investigated. A vitamin D‑deficient mouse model was established, and bone marrow‑derived DCs (BMDCs) were isolated and treated with GM‑CSF and interleukin (IL)‑4 for 6 days, followed by an additional 24 h of treatment with Bacillus Calmette‑Guérin (BCG). The expression levels of surface molecules of DCs, including integrin alpha‑X and T‑lymphocyte activation antigen CD86, were significantly increased by BCG in the vitamin D‑deficient mice model group compared with the control group, while those of T‑lymphocyte activation antigen CD80, major histocompatibility complex class I and major histocompatibility complex class II were significantly decreased. These changes were BCG concentration‑dependent. In addition, the levels of IL‑4, IL‑6 and IL‑10 in the BMDCs from the vitamin D‑deficient mice were significantly decreased compared with the control mice, while the levels of tumor necrosis factor‑α, IL‑5, IL‑2, IL‑12 and interferon‑γ were significantly increased. Furthermore, the expression levels of vitamin D receptor (VDR) and CYP27B1 protein in the BMDCs from the vitamin D‑deficient mice were decreased compared with the control. BCG significantly increased the expression levels of VDR and CYP27B1 in the BMDCs. The DCs treated with BCG significantly induced the viability of CD4+ T lymphocytes. Therefore, BCG increases DCs and may enhance immunofunction, which may assist in preventing the risk of tuberculosis in patients with a vitamin D deficiency.