The Journal of international medical research · 2020
Bacillus Calmette-Guérin (BCG) stimulates changes in dendritic cell surface marker expression in vitamin D-deficient mice.
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Yang Huifeng, Zhan Yang, Wu Haotian, Xiang Liangbi
Аннотация
OBJECTIVE: Vitamin D (VD) deficiency increases susceptibility to tuberculosis and is an important immunomodulator. Dendritic cells (DCs) are important antigen-presenting cells that play a critical role during tuberculosis infection, and Mycobacterium tuberculosis modulates DC responses. The underlying mechanism is poorly understood. Our aim was to study changes in DC surface markers in VD deficient mice administered Bacillus Calmette-Guérin (BCG).
METHODS: We divided C57BL/6 mice into a normal group and a VD deficient group. Two groups of mouse bone marrow-derived cells were isolated and cultured with granulocyte-macrophage colony-stimulating factor (20 ng/mL) and interleukin-4 (10 ng/mL) for 6 days. On day 7, BCG (0, 1 or 2 mg/mL) was administered to both groups for 24 hours. Non-adherent cells were harvested to assess DC phenotypic changes induced by different concentrations of BCG.
RESULTS: Expression levels of CD80, MHC-I, MHC-II and CD86 on the surfaces of DCs from VD deficient mice were lower than those in DCs from normal mice. By contrast, the expression level of CD11c on DCs was higher in VD deficient mice than in normal mice. Changes in all factors were concentration-dependent.
CONCLUSIONS: These findings indicate that BCG reduced DC surface marker expression to modulate immune responses during M. tuberculosis infection.
METHODS: We divided C57BL/6 mice into a normal group and a VD deficient group. Two groups of mouse bone marrow-derived cells were isolated and cultured with granulocyte-macrophage colony-stimulating factor (20 ng/mL) and interleukin-4 (10 ng/mL) for 6 days. On day 7, BCG (0, 1 or 2 mg/mL) was administered to both groups for 24 hours. Non-adherent cells were harvested to assess DC phenotypic changes induced by different concentrations of BCG.
RESULTS: Expression levels of CD80, MHC-I, MHC-II and CD86 on the surfaces of DCs from VD deficient mice were lower than those in DCs from normal mice. By contrast, the expression level of CD11c on DCs was higher in VD deficient mice than in normal mice. Changes in all factors were concentration-dependent.
CONCLUSIONS: These findings indicate that BCG reduced DC surface marker expression to modulate immune responses during M. tuberculosis infection.