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Influence of eicosapentaenoic acid, an omega-3 fatty acid, on ultraviolet-B generation of prostaglandin-E2 and proinflammatory cytokines interleukin-1 beta, tumor necrosis factor-alpha, interleukin-6 and interleukin-8 in human skin in vivo.
Photochem Photobiol. 2004 Sep-Oct; 80(2):231-5.PP

Abstract

Dietary omega-3 polyunsaturated fatty acids (omega-3 PUFA) reduce sunburn, an acute inflammatory response, in humans. We assessed whether this may be mediated by reduced ultraviolet-B (UV-B) induction of proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, IL-6, IL-8 and prostaglandin (PG)E(2) in healthy skin. In a double-blind, randomized study, 28 humans received 4 g daily of 95% ethyl esters of eicosapentaenoic acid (EPA) or oleic acid (OA) orally for 3 months. Skin biopsies and suction blister fluid were taken from unexposed and UV-B-exposed skin and examined for mediator expression immunohistochemically and quantitatively by immunoassay; plasma levels were also assayed. The subjects taking EPA, but not OA, showed a significant rise in their minimal erythemal dose (MED) (data reported elsewhere). Before supplementation, irradiation with 3x MED UV-B increased blister fluid TNF-alpha, IL-6, IL-8 and PGE(2) at 16 h (all P < 0.001). No significant change occurred in baseline or UV-B-induced skin levels of cytokines after either supplement, whereas UV-B induction of PGE(2) was abolished after EPA but not OA. Immunohistochemical expression of the cytokines at baseline and after UV-B was unaltered by EPA and OA; circulating cytokine and PGE(2) levels were also unchanged. Hence, in healthy skin in vivo, there was no evidence that reduction of the sunburn response by EPA is mediated by the proinflammatory cytokines examined; abrogation of UV-B-generated PGE(2) may play a role.

Authors+Show Affiliations

Photobiology Unit, Dermatology Centre, University of Manchester, Manchester M6 8HD, UK.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15362934

Citation

Shahbakhti, Hassan, et al. "Influence of Eicosapentaenoic Acid, an Omega-3 Fatty Acid, On ultraviolet-B Generation of prostaglandin-E2 and Proinflammatory Cytokines Interleukin-1 Beta, Tumor Necrosis Factor-alpha, Interleukin-6 and Interleukin-8 in Human Skin in Vivo." Photochemistry and Photobiology, vol. 80, no. 2, 2004, pp. 231-5.
Shahbakhti H, Watson RE, Azurdia RM, et al. Influence of eicosapentaenoic acid, an omega-3 fatty acid, on ultraviolet-B generation of prostaglandin-E2 and proinflammatory cytokines interleukin-1 beta, tumor necrosis factor-alpha, interleukin-6 and interleukin-8 in human skin in vivo. Photochem Photobiol. 2004;80(2):231-5.
Shahbakhti, H., Watson, R. E., Azurdia, R. M., Ferreira, C. Z., Garmyn, M., & Rhodes, L. E. (2004). Influence of eicosapentaenoic acid, an omega-3 fatty acid, on ultraviolet-B generation of prostaglandin-E2 and proinflammatory cytokines interleukin-1 beta, tumor necrosis factor-alpha, interleukin-6 and interleukin-8 in human skin in vivo. Photochemistry and Photobiology, 80(2), 231-5.
Shahbakhti H, et al. Influence of Eicosapentaenoic Acid, an Omega-3 Fatty Acid, On ultraviolet-B Generation of prostaglandin-E2 and Proinflammatory Cytokines Interleukin-1 Beta, Tumor Necrosis Factor-alpha, Interleukin-6 and Interleukin-8 in Human Skin in Vivo. Photochem Photobiol. 2004 Sep-Oct;80(2):231-5. PubMed PMID: 15362934.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Influence of eicosapentaenoic acid, an omega-3 fatty acid, on ultraviolet-B generation of prostaglandin-E2 and proinflammatory cytokines interleukin-1 beta, tumor necrosis factor-alpha, interleukin-6 and interleukin-8 in human skin in vivo. AU - Shahbakhti,Hassan, AU - Watson,Rachel E B, AU - Azurdia,Richard M, AU - Ferreira,Christiana Z, AU - Garmyn,Marjan, AU - Rhodes,Lesley E, PY - 2004/9/15/pubmed PY - 2006/4/11/medline PY - 2004/9/15/entrez SP - 231 EP - 5 JF - Photochemistry and photobiology JO - Photochem Photobiol VL - 80 IS - 2 N2 - Dietary omega-3 polyunsaturated fatty acids (omega-3 PUFA) reduce sunburn, an acute inflammatory response, in humans. We assessed whether this may be mediated by reduced ultraviolet-B (UV-B) induction of proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta, IL-6, IL-8 and prostaglandin (PG)E(2) in healthy skin. In a double-blind, randomized study, 28 humans received 4 g daily of 95% ethyl esters of eicosapentaenoic acid (EPA) or oleic acid (OA) orally for 3 months. Skin biopsies and suction blister fluid were taken from unexposed and UV-B-exposed skin and examined for mediator expression immunohistochemically and quantitatively by immunoassay; plasma levels were also assayed. The subjects taking EPA, but not OA, showed a significant rise in their minimal erythemal dose (MED) (data reported elsewhere). Before supplementation, irradiation with 3x MED UV-B increased blister fluid TNF-alpha, IL-6, IL-8 and PGE(2) at 16 h (all P < 0.001). No significant change occurred in baseline or UV-B-induced skin levels of cytokines after either supplement, whereas UV-B induction of PGE(2) was abolished after EPA but not OA. Immunohistochemical expression of the cytokines at baseline and after UV-B was unaltered by EPA and OA; circulating cytokine and PGE(2) levels were also unchanged. Hence, in healthy skin in vivo, there was no evidence that reduction of the sunburn response by EPA is mediated by the proinflammatory cytokines examined; abrogation of UV-B-generated PGE(2) may play a role. SN - 0031-8655 UR - https://www.unboundmedicine.com/medline/citation/15362934/Influence_of_eicosapentaenoic_acid_an_omega_3_fatty_acid_on_ultraviolet_B_generation_of_prostaglandin_E2_and_proinflammatory_cytokines_interleukin_1_beta_tumor_necrosis_factor_alpha_interleukin_6_and_interleukin_8_in_human_skin_in_vivo_ DB - PRIME DP - Unbound Medicine ER -