Marine n-3 polyunsaturated fatty acids (PUFAs) may influence inflammation through a variety of mechanisms; many of these are mediated by, or at least associated with, changes in fatty acid composition of inflammatory cell membranes. Changes in fatty acid composition can modify membrane fluidity, cell signaling mechanisms leading to altered gene expression, and the pattern of lipid mediator production. Human inflammatory cells are typically rich in the n-6 fatty acid arachidonic acid, but the contents of arachidonic acid and of the n-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) can be altered through oral administration of EPA and DHA. Eicosanoids produced from arachidonic acid (e.g. prostaglandin E2) have roles in inflammation. EPA also gives rise to eicosanoids and these may have differing properties from those of arachidonic acid-derived eicosanoids, often being less potent. EPA and DHA give rise to resolvins which are anti-inflammatory and inflammation resolving. Increased membrane content of EPA and DHA (and decreased arachidonic acid content) results in a changed pattern of production of eicosanoids and probably also of resolvins. Changing the fatty acid composition of inflammatory cells also affects the production of peptide mediators of inflammation (cytokines, adhesion molecules etc.). Thus, the fatty acid composition of human inflammatory cells influences their function; the contents of arachidonic acid, EPA and DHA appear to be especially important. The anti-inflammatory actions of marine n-3 PUFAs suggest that they may be of therapeutic use in diseases involving chronic inflammation.

View full abstract