Effect of vitamin D3 on chemokine expression in pulmonary tuberculosis

Abstract 1,25 Dihydroxy vitamin D 3 (vitamin D 3 ) is an immunomodulator and its deficiency has been associated with susceptibility to tuberculosis. We have studied the immunoregulatory role of vitamin D 3 on various chemokine expression in pulmonary tuberculosis. Peripheral blood mononuclear cells obtained from 21 pulmonary tuberculosis (PTB) patients and 24 healthy controls (HCs) were cultured for 48 h with culture filtrate antigen (CFA) of Mycobacterium tuberculosis with or without vitamin D 3 at a concentration 1 × 10 −7  M. The relative mRNA expression of monocyte chemoattractant protein-1 (MCP-1, CCL2), macrophage inflammatory protein-1α (MIP-1α, CCL3), macrophage inflammatory protein-1β (MIP-1β, CCL4), and regulated upon-activation, normal T cell-expressed and secreted (RANTES, CCL5) and IFN-γ inducible protein-10 (IP-10, CXCL10) chemokines were estimated from 48 h old macrophages using real-time polymerase chain reaction (RT-PCR). The culture supernatants were used to estimate the various chemokines including monokine induced by IFN-γ (MIG, CXCL9) levels using cytometric bead array. In HCs, vitamin D 3 significantly suppressed the MCP-1 mRNA expression of CFA stimulated cells ( p  = 0.0027), while no such effect was observed in PTB patients. Vitamin D 3 showed no significant effect on MIP-1α, MIP-1β and RANTES in both the study groups. The CFA induced IP-10 mRNA and protein expression was significantly suppressed by vitamin D 3 in both the study groups ( p 3 was observed with MIG protein in healthy controls ( p  = 0.0029) and a trend towards a suppression was observed in PTB patients. The suppressive effect of vitamin D 3 is more prominent in CXC chemokines rather than CC chemokines. This suggests that vitamin D 3 may down regulate the recruitment and activation of T-cells through CXC chemokines at the site of infection and may act as a potential anti-inflammatory agent.