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Carcinogenesis Advance Access originally published online on March 26, 2007
Carcinogenesis 2007 28(6):1329-1333; doi:10.1093/carcin/bgm065
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© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Conjugated linoleic acids modulate UVR-induced IL-8 and PGE2 in human skin cells: potential of CLA isomers in nutritional photoprotection

Amy Storey, Julia S. Rogers1, Francis McArdle, Malcolm J. Jackson and Lesley E. Rhodes2,*

Department of Medicine, University of Liverpool, Liverpool UK
1 Unilever Research Laboratories, Bedford, UK
2 Photobiology Unit, Dermatological Sciences, University of Manchester, Salford Royal Foundation Hospital, Manchester M6 8HD, UK

* To whom correspondence should be addressed. Tel: +44 161 206 1150; Fax: +44 161 206 1156; Email lesley.e.rhodes{at}manchester.ac.uk

Conjugated linoleic acids (CLA), derivatives of linoleic acid found in food products, inhibit chemically induced skin cancers in mice. However, their potential photoprotective properties remain unexplored. We examined whether CLA may modulate ultraviolet radiation (UVR)-induced secretion of interleukin (IL)-8 and prostaglandin E2 (PGE2), mediators implicated in UVR-induced inflammation and carcinogenesis, in human skin cells. Since tumour necrosis factor (TNF)-{alpha} is an early mediator of UVR effects, we also examined influence of CLA on TNF-{alpha}-induced mediator release. HaCaT keratinocytes were supplemented with CLA isomers cis-9-trans-11 (c9,t11-CLA; ≥90%), trans-10-cis-12 (t10,c12-CLA; ≥90%) or all trans-trans isomers (tt-CLA; 23.7%) in tetrahydrofuran/fetal calf serum (THF/FCS) or THF/FCS control. Supplementation of keratinocytes with c9,t11-CLA reduced Ultraviolet B(UVB)-induced IL-8 from 37 113 ± 2903 pg/ng protein in control cells to 14 167 ± 2063 pg/ng protein (P < 0.001). Similarly, t10,c12-CLA reduced UVB-induced IL-8 to 9786 ± 1291.5 pg/ng protein (P < 0.001). Additionally, t10,c12-CLA and tt-CLA inhibited TNF-{alpha}-induced IL-8 from 11 669 ± 1692 pg/ng protein in control cells to 5540 ± 191 (P < 0.001) and 8082 ± 1298 pg/ng (P < 0.01) protein, respectively. UVB-induced PGE2 release was reduced by tt-CLA supplementation, from 4.8 ± 1.2 to 1.6 ± 0.8 pg/mg protein (P < 0.01), but increased by t10,c12-CLA to 8.8 ± 1 pg/mg protein (P < 0.001). Influence of CLA on UVB-induced PGE2 release was further explored in CCD922SK dermal fibroblasts. CLA isomers reduced UVB-induced PGE2 in fibroblasts, reaching significance with c9,t11-CLA (98 ± 5 falling to 0 pg/mg protein, P < 0.05). Hence, CLA isomers differentially modulate UVB effects on skin cells in vitro. CLA-containing foods have potential in photoprotection; the cutaneous effects of individual isomers warrant clinical study.

Abbreviations: CLA, conjugated linoleic acid; c9,t11, cis-9-trans-11; FA, fatty acids; FCS, fetal calf serum; IL, interleukin; LA, linoleic acid; OA, oleic acid; PGE2, prostaglandin E2; t10,c12, trans-10-cis-12; THF, tetrahydrofuran; TNF, tumour necrosis factor; tt, trans-trans; UVR, ultraviolet radiation

Received November 8, 2007; revised March 16, 2007; accepted March 16, 2007.


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