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Induction of cathelicidin-mediated antimicrobial pathway against intracellular  M. tuberculosis  by 1,25-dihydroxyvitamin D 3  (1,25(OH) 2 D 3 ), the active form of vitamin D, has been documented  in vitro . However, in  in vivo  studies related to inflammatory disorders, 1,25(OH) 2 D 3  has been demonstrated to induce an anti-inflammatory response. We therefore examined whether in the murine model of tuberculosis, the anti-inflammatory effects of 1,25(OH) 2 D 3  would affect the outcome of  M. tuberculosis  infection. We show here that administration of 1,25(OH) 2 D 3  to  M. tuberculosis  infected mice led to a change in lung granuloma architecture, characterized by a marked decrease in B cell lymphocytic aggregates. Consistent with the altered granulomas, 1,25(OH) 2 D 3 -treated mice also exhibited significantly higher bacterial burden in the lungs compared to the control group. These findings highlight the need to further investigate the effect of vitamin D on host immunity to  M. tuberculosis  in the context of the granulomatous response.

1,25 (OH)2D3 treatment alters the granulomatous response in M. tuberculosis infected mice