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Long chain fatty acids and gene expression in inflammation and immunity

Calder, Philip C.

Current Opinion in Clinical Nutrition and Metabolic Care: July 2013 - Volume 16 - Issue 4 - p 425–433
doi: 10.1097/MCO.0b013e3283620616
GENES AND CELL METABOLISM: Edited by Lynette R. Ferguson and Philip Newsholme

Purpose of review The purpose of this review is to discuss recent studies reporting on the influence of fatty acids on gene expression in relation to inflammation and immune responses.

Recent findings Saturated fatty acids promote, whereas several n-3 fatty acids, in particular eicosapentaenoic and docosahexaenoic acids, some isomers of conjugated linoleic acid, and punicic acid suppress, expression of inflammatory genes. The most common targets of fatty acids are genes encoding cytokines, chemokines, cyclooxygenase, nitric oxide synthase, and matrix metalloproteinases. The anti-inflammatory actions of fatty acids often involve inhibition of activation of nuclear factor-κB and activation of peroxisome proliferator-activated receptors α and γ. Common upstream events include actions on Toll-like receptors and via G-protein coupled receptors. Fatty acids can influence expression of genes involved in immune and inflammatory cell development and differentiation. Recent studies using genome-wide analyses demonstrate that dietary fatty acids can alter expression of a large number (many hundreds) of genes in human peripheral blood mononuclear cells.

Summary A wide range of fatty acids alter expression of genes involved in development, differentiation, and function of cells involved in inflammation and immunity.

Human Development and Health Academic Unit, Faculty of Medicine, University of Southampton, Southampton, UK

Correspondence to Philip C. Calder, Human Development and Health Academic Unit, Faculty of Medicine, University of Southampton, Institute of Developmental Sciences Building, MP887 Southampton General Hospital, Tremona Road, Southampton SO16 6YD, UK. Tel: +44 2380 795 250; fax: +44 2380 795 255; e-mail:

© 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins