The effect of ultraviolet B‐induced vitamin D levels on host resistance to Mycobacterium tuberculosis: a pilot study in immigrant Asian adults living in the United Kingdom

Abstract

Asian immigrants to the United Kingdom demonstrate much higher tuberculosis rates than the indigenous population. This is postulated to be because of their low vitamin D levels, consequent upon a combination of diet and their reduced ultraviolet (UV) exposure in the United Kingdom, because vitamin D enhances antimycobacterial activity in in vitro systems. The aim of this study was to examine the relationship between UVB exposure, vitamin D levels and tuberculo-immunity in Asian immigrants in the United Kingdom. Suberythemal UVB treatments were given to eight subjects on 3 consecutive days, using broadband UVB fluorescent lamps. Blood was sampled for 25-hydroxyvitamin D (25-OH D) and whole blood functional assays were performed for antimycobacterial immunity. The mean 25-OH D level increased from a baseline of 11.23 ng/ml (95% CI 6.7-20.39) to 20.39 ng/ml (95% CI 16.6-20) following UVB treatment, P<0.01. However, no significant change in antimycobacterial immunity occurred following UVB exposure. This pilot study in Asian subjects with good baseline tuberculo-immunity has not supported a role for UVB-induced 25-OH D in the immune response to Mycobacterium tuberculosis.

Vitamin D, tuberculin skin test conversion, and latent tuberculosis in Mongolian school-age children: a randomized, double-blind, placebo-controlled feasibility trial

“…According to this measure, vitamin D supplementation suppressed bacterial growth at 24 h, an indicator of innate immunity, by 20.4% more than placebo (P = 0.03) but did not affect luminescence or interferon-g secretion at 96 h-an indicator of acquired immunity. On the other hand, in a study by Yesudian et al (30), significant change in antimycobacterial immunity (as expressed by the BCG-lux assay) did not occur even though the mean 25(OH)D concentration increased significantly after ultraviolet B treatment (P , 0.01).…”

Reversing Bacteria‐induced Vitamin D Receptor Dysfunction Is Key to Autoimmune Disease

“…Although there is some evidence that raising 25‐D levels fuels innate immune function by increasing the availability of precursor 25‐D to be converted to 1,25‐D, 10,33 the results are not consistent, 34 and further studies are needed. Even if this were to be confirmed in the healthy general population, however, it would not necessarily be true for those who already have bacteria‐induced VDR dysfunction.…”

Vitamin D Metabolites as Clinical Markers in Autoimmune and Chronic Disease

“…[1][2][3][4][5][6][7][8] However, other studies have shown a deleterious or no beneficial effect of vitamin D supplementation on certain diseases. [9][10][11][12][13][14][15][16][17][18] The effects of vitamin D are the result of genomic and nongenomic actions mediated by the active form of vitamin D, termed calcitriol, which is also known as 1,25-dihydroxyvitamin D3 (1,25-D). Yet most of the studies evaluating vitamin D and its association with disease are based on 25-hydroxyvitamin D (25-D) serum levels and not 1,25-D.…”

“…There is increasing interest in the role of vitamin D deficiency in a number of chronic health problems, including autoimmune diseases 1–8 . However, other studies have shown a deleterious or no beneficial effect of vitamin D supplementation on certain diseases 9–18 . The effects of vitamin D are the result of genomic and non‐genomic actions mediated by the active form of vitamin D, termed calcitriol, which is also known as 1,25‐dihydroxyvitamin D3 (1,25‐D).…”