Effect of oral eicosapentaenoic acid on epidermal Langerhans cell numbers and PGD2 production in UVR-exposed human skin: a randomised controlled study

Abstract

Langerhans cells (LC) are sentinels of skin's immune system, their loss from epidermis contributing to UVR-suppression of cell mediated immunity (CMI). Omega-3 polyunsaturated fatty acids show potential to abrogate UVR-suppression of CMI in mice and humans, potentially through modulation of LC migration. Our objectives were to examine if eicosapentaenoic acid (EPA) ingestion influences UV-mediated effects on epidermal LC numbers and levels of immunomodulatory mediators including prostaglandin (PG)D₂, which is expressed by LC.

In a double-blind randomised controlled study, healthy individuals took 5g EPA-rich (n=40) or control (n=33) lipid for 12-weeks; UVR exposed and unexposed skin samples were taken pre- and post-supplementation. Epidermal LC numbers were assessed by immunofluorescence for CD1a, and skin blister fluid PG and cytokines quantified by LC-MS/MS and Luminex assay, respectively. Pre-supplementation, UVR reduced mean (SEM) LC number/mm² from 913 (28) to 322 (40) (p<0.001), and mean PGD₂ level by 37% from 8.1 (11.6) to 5.1 (5.6) pg/μl; p<0.001), while IL-8 level increased (p<0.001). Despite confirmation of EPA bioavailability in red blood cells and skin in the active group, no between-group effect of EPA was found on UVR-modulation of LC numbers, PGD₂ or cytokine levels post-supplementation.

Thus no evidence was found for EPA abrogation of photoimmunosuppression through an impact on epidermal LC numbers. Intriguingly, UVR-exposure substantially reduced cutaneous PGD₂ levels in humans, starkly contrasting with reported effects of UVR on other skin PG. Lowered PGD₂ levels could reflect LC loss from the epidermis and/or altered dendritic cell activity, and may be relevant for phototherapy of skin disease.

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