Vitamin D supplementation as preventive strategy for Tuberculosis

Introduction: Tuberculosis (TB) is a serious worldwide health concern. About thirty percent of the world population is infected with Mycobacterium tuberculosis which is the causative agent of TB. Immunomodulation through dietary supplementation has been widely used as a mechanism to enhance the immune system.


Vitamin D mediates activation of the innate immune system in macrophages which prepare the primary line of defense against infection. After micro-organism detection, toll like receptors (TLR) on the phagocyte membrane is activated to induce transcriptional up-regulation of the vitamin D receptor (VDR) and accountable for the VDR-dependent regulation responsible for the up-regulation of cathelicidin expression. Several studies demonstrate the impact of calcidiol levels, VDR polymorphisms and vitamin D supplementation on the acquisition of TB and the outcomes of TB infections.


Increased risk of TB was reported among the people with lower vitamin D levels. Vitamin D supplementation seems to have a positive consequence on TB outcomes. Human monocytes have receptors for 1, 25 dihydroxyvitamin D that activates antimycobacterial responses in human monocytes and macrophages by enhancing phagocytosis and granuloma formation. Calcitriol induces anti mycobacterial activity in vitro. This metabolite modulates the host response to Mycobacterial infection by induction of reactive nitrogen and oxygen intermediate suppression of matrix metalloproteinase enzymes implicated in the pathogenesis of pulmonary cavitation and induction of anti microbial peptide catheliciden which induces autophagy.

Tuberculosis, HIV and Vitamin D:

Possible mechanisms to explain the association between 25(OH)D deficiency and higher severity of TB & HIV disease: Firstly, Chronic inflammation due the infection and subsequent TNF-饾浖 overproduction may be responsible for renal 1饾浖-hydroxylase impairment, reducing the PTH (parathyroid hormone) stimulatory effect on the production of the hormonally active 1,25(OH)2D (1,25-dihydroxyvitamin D). Second, Infectious complications as a result of poor immunity require hospital care, which significantly reduces the duration of sun exposure for patients. Third, Antituberculous drugs (rifampicin, izoniazide, ethambutol, and pyrazinamide) and ART (anti retro viral therapy; Effavirenz, Ritonavir) affect metabolism of Vitamin D.


It may reduce the expression of cytocrome P450 enzyme (Cyp2R1) which is involved in converting vitamin D3 to 25(OH)D and also unregulated Cyp24 which convert active vitamin D to inactive metabolites and also could inhibits 1伪 & 25伪 hydroxylation, which inhibit to form active form of Vitamin D (1, 25(OH2) D) from 25(OH) D.



Key Points:

Observational studies indicate that individuals infected with pulmonary TB with low vitamin D status may be at increased risk of mortality and mental illness.

Vitamin D supplementation enhances the adherence of antituberculosis drugs, CD4 count, Immune system of the body and decline the chances of mental disorders.

Several studies demonstrate the impact of calcidiol levels, VDR polymorphisms, and vitamin D supplementation on the acquisition of TB and the outcomes of TB infections.

Activated Toll-like receptors induce transcriptional up-regulation of the vitamin D receptor (VDR). VDR-dependent regulation of a variety of genes including the up-regulation of cathelicidinin expression.

Incorporation of cathelidicin into phagosomes containing internalized M. tuberculosis which enable to kill the invading pathogen.

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