| Vitamin A |
Inhibits multiplication of virulent bacilli in cultured human macrophages; plays a vital role in lymphocyte proliferation and in maintaining the function of epithelial tissues, and normal functioning of T and B lymphocytes, macrophage activity, and generation of an antibody response. |
[71, 72] |
| Vitamin D |
Plays a role in the function of macrophages, key factor in host resistance to tuberculosis; genetic variations in the vitamin D receptor were identified as a major determinant of the risk for tuberculosis. |
[72, 73] |
| Vitamin E |
In numerous studies, vitamin E concentration was found to be significantly lower in tuberculosis patients than it was in healthy controls and concentrations of the antioxidant vitamins A, C, and E were significantly lower in tuberculosis patients. |
[74] |
| Vitamin C |
The bactericidal activity of vitamin C against Mycobacterium tuberculosis is dependent on high ferrous ion levels and reactive oxygen species production, and causes a pleiotropic effect on several biological processes. Concentrations of antioxidant vitamins A, C, and E were significantly lower in tuberculosis patients than they were in healthy patients. |
[54, 74] |
| Iron |
Iron is essential for sustaining the life of most organisms including mycobacteria. Iron can be highly toxic because it catalyzes the generation of reactive oxygen species from normal products of aerobic respiration via the Harber-Weiss and Fenton reactions. Anemia resulting from chronic infection and/or iron deficiency could increase susceptibility to infections such as tuberculosis. |
[75, 76, 77] |
| Copper |
Copper is a trace element that is essential for the growth and development of almost all organisms including bacteria. Copper overload in most systems is toxic. Copper accumulates in phagosomes of macrophage infected with bacteria, suggesting that copper is involved an innate immune mechanism to combat invading pathogens. |
[77, 78, 79] |
| Zinc |
Decreased phagocytosis and a reduced number of circulating T-cells and reduced tuberculin reactivity are observed at least in animals with zinc deficiency. Zinc may also limit free-radical membrane damage during inflammation. The mechanisms of zinc ion toxicity may also include inactivation of iron-sulfur clusters and inhibition of manganese uptake through transport competition in the bacterial periplasm. Zinc has an essential role in vitamin A metabolism. |
[72, 77, 78, 79] |
| Selenium |
Maintains immune processes and may play a critical role in the clearance of mycobacteria by both cell-mediated and humoral immunity. Selenium has been reported to be significant factor in developing mycobacterial diseases in HIV-positive patients. |
[72, 80] |
| Cobalt |
Cobalt is required for the biosynthesis of vitamin B12 and is an essential micronutrient for both M. tuberculosis and its host. Recent metal-based drugs that utilize coordination complexes of copper and cobalt have been reported to have notable selectivity and marked potency against M. tuberculosis, which suggests these metals are important for controlling tuberculosis infection. |
[79, 81] |
| Cholesterol |
Hypocholesterolemia is prevalent in tuberculosis patients. Decreased cholesterol levels have been reported to be associated with mortality in miliary tuberculosis patients. |
[72, 81, 82] |
| Manganese |
Manganese cations play a catalytic role in numerous proteins and are important in mediating resistance to oxidative stress. Manganese cation chelation by calprotectin inhibits bacterial defenses against superoxide. |
[77, 79] |
