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Omega-3 fatty acids and inflammatory processes

Omega-3 fatty acids and inflammatory processes
Omega-3 fatty acids and inflammatory processes
Long chain fatty acids influence inflammation through a variety of mechanisms;
many of these are mediated by, or at least associated with, changes in fatty acid
composition of cell membranes. Changes in these compositions can modify membrane
fluidity, cell signaling leading to altered gene expression, and the pattern of lipid mediator
production. Cell involved in the inflammatory response 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 have roles
in inflammation. EPA also gives rise to eicosanoids and these often have differing
properties from those of arachidonic acid-derived eicosanoids. EPA and DHA give rise to
newly discovered 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 resolvins. Changing the fatty
acid composition of cells involved in the inflammatory response also affects production of
peptide mediators of inflammation (adhesion molecules, cytokines etc.). Thus, the fatty
acid composition of cells involved in the inflammatory response influences their function;
the contents of arachidonic acid, EPA and DHA appear to be especially important. The
anti-inflammatory effects of marine n-3 PUFAs suggest that they may be useful as
therapeutic agents in disorders with an inflammatory component.
leukocyte, neutrophil, macrophage, monocyte, eicosanoid, cytokine, interleukin, fish oil
355-374
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6

Calder, Philip C. (2010) Omega-3 fatty acids and inflammatory processes. Nutrients, 2 (3), 355-374. (doi:10.3390/nu2030355).

Record type: Review

Abstract

Long chain fatty acids influence inflammation through a variety of mechanisms;
many of these are mediated by, or at least associated with, changes in fatty acid
composition of cell membranes. Changes in these compositions can modify membrane
fluidity, cell signaling leading to altered gene expression, and the pattern of lipid mediator
production. Cell involved in the inflammatory response 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 have roles
in inflammation. EPA also gives rise to eicosanoids and these often have differing
properties from those of arachidonic acid-derived eicosanoids. EPA and DHA give rise to
newly discovered 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 resolvins. Changing the fatty
acid composition of cells involved in the inflammatory response also affects production of
peptide mediators of inflammation (adhesion molecules, cytokines etc.). Thus, the fatty
acid composition of cells involved in the inflammatory response influences their function;
the contents of arachidonic acid, EPA and DHA appear to be especially important. The
anti-inflammatory effects of marine n-3 PUFAs suggest that they may be useful as
therapeutic agents in disorders with an inflammatory component.

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More information

Published date: March 2010
Keywords: leukocyte, neutrophil, macrophage, monocyte, eicosanoid, cytokine, interleukin, fish oil

Identifiers

Local EPrints ID: 188715
URI: http://eprints.soton.ac.uk/id/eprint/188715
PURE UUID: f5c01063-4c2c-46da-a0aa-db9fe2f25856
ORCID for Philip C. Calder: ORCID iD orcid.org/0000-0002-6038-710X

Catalogue record

Date deposited: 27 May 2011 08:55
Last modified: 15 Mar 2024 02:50

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