The eicosanoid response to high dose UVR exposure of individuals prone and resistant to sunburn.

High personal UVR doses can be gained during leisure activities, causing intense self-resolving inflammation (sunburn) of unprotected skin. UVR activates release of membrane fatty acids and upregulates their metabolism by cyclooxygenases (COX) and lipoxygenases (LOX) to different eicosanoids. While COX-derived prostaglandin (PG)E(2) is a potent mediator of sunburn vasodilatation, LOX-derived 15-hydroxyeicosatetraenoic acid (HETE) and its lipoxin metabolites may contribute to sunburn limitation. We explored the relationships between expression of these lipid mediators and the clinical and histological outcomes, comparing responses of individuals prone and more resistant to sunburn. An acute UVR exposure of 12 SED (standard erythema dose) was applied to buttock skin of 32 white Caucasians (n = 16 phototype I/II, n = 16 phototype III/IV), and over the subsequent 72 h assessments were made of skin erythema, immunohistochemical expression of leukocyte markers, COX-2, 12-LOX, 15-LOX and nitric oxide synthase (NOS), and eicosanoid levels by LC/ESI-MS/MS. Evidence of a significant inflammatory response was seen earlier in phototype I/II with regard to expression of erythema (4 h, p < 0.001), neutrophil infiltration (24 h, p = 0.01), epidermal COX-2 (24 h, p < 0.05) and 12-LOX (24 h, p < 0.01), and dermal eNOS (24 h, p < 0.05) proteins, although CD3+ lymphocyte infiltration showed an earlier increase in phototype III/IV (24 h, p < 0.05). Although erythema was equivalent at 72 h in both groups, phototype I/II showed higher PGE(2) accompanied by elevated 15-HETE, and a strong positive correlation was seen between these mediators (n = 18, r = 0.805, p = 0.0001). Hence anti-inflammatory eicosanoid 15-HETE may temper the pro-inflammatory milieu in sunburn, having greater influence in those prone to sunburn than those more resistant, given the same high UVR exposure conditions.

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.

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.