Polyunsaturated fatty acids and inflammatory processes: New twists in an old tale
Abstract
The n-6 fatty acid arachidonic acid (AA; 20:4n-6) gives rise to eicosanoid mediators that have established roles in inflammation and AA metabolism is a long recognised target for commonly used anti-inflammatory therapies. It has generally been assumed that all AA-derived eicosanoids are pro-inflammatory. However this is an over-simplification since some actions of eicosanoids are anti-inflammatory (e.g. prostaglandin (PG) E(2) inhibits production of some inflammatory cytokines) and it has been discovered quite recently that PGE(2) inhibits production of inflammatory leukotrienes and induces production of inflammation resolving lipoxin A(4). The n-3 fatty acids from oily fish and "fish oils", eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3), are incorporated into inflammatory cell phospholipids in a time- and dose-dependent manner. They are incorporated partly at the expense of AA, but also of other n-6 fatty acids. EPA and DHA inhibit AA metabolism. Thus production of AA-derived eicosanoids is decreased by these n-3 fatty acids; this occurs in a dose-dependent manner. EPA gives rise to an alternative family of eicosanoids (e.g. PGE(3)), which frequently, but not always, have lower potency than those produced from AA. Recently a new family of EPA- and DHA-derived lipid mediators called resolvins (E- and D-series) has been described. These have potent anti-inflammatory and inflammation resolving properties in model systems. It seems likely that these mediators will explain many of the antiinflammatory actions of n-3 fatty acids that have been described. In addition to modifying the profile of lipid-derived mediators, fatty acids can also influence peptide mediator (i.e. cytokine) production. To a certain extent this action may be due to the altered profile of regulatory eicosanoids, but it seems likely that eicosanoid-independent actions are a more important mechanism. Indeed effects on transcription factors that regulate inflammatory gene expression (e.g. nuclear factor kappaB) seem to be important.
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EPA and DHA can inhibit endogenous production of pro-inflammatory arachidonic acids by competing as substrates for enzymes during eicosanoid synthesis.
“EPA and DHA can also inhibit the endogenous production of pro-inflammatory arachidonic acids by competing as substrates for the enzymes during eicosanoid synthesis [66,67].”
From Potential Roles of n-3 PUFAs during Skeletal Muscle Growth and Regeneration (2018) · cites this paper as [67]
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Self-citation
- Authors
- Calder, P. C.
- Affiliations
- Southampton General Hospital (GB)
- Corresponding author
- Calder, Philip C.
- ORCID
- Calder, Philip C.
- Venue
- Biochimie
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 91
- Issue
- 6
- Pages
- 791-795
- ISSN
- 0037-9042 (ISSN-L)
- 0300-9084
- OpenAlex
- W2059751934
- Cited by
- 721
- References
- 56
- Citations by year
- 2026: 19 · 2025: 18 · 2024: 25 · 2023: 23 · 2022: 32 · 2021: 35 · 2020: 36 · 2019: 38 · 2018: 37 · 2017: 50 · 2016: 41 · 2015: 46 · 2014: 70 · 2013: 65 · 2012: 65
- FWCI
- 7.10
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochimie (publishedVersion)
- PubMed (publishedVersion)
- ePrints Soton (University of Southampton) (submittedVersion)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Health Sciences › Medicine › Pharmacology › Inflammatory mediators and NSAID effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- polyunsaturated fatty acids, arachidonic acid, eicosanoids, omega-3 fatty acids, eicosapentaenoic acid, docosahexaenoic acid, resolvins, prostaglandin E2, leukotrienes, lipoxin A4, anti-inflammatory lipid mediators, inflammation resolution, cytokine production, NF-κB, eicosanoid metabolism
- MeSH terms
- Animals, Anti-Inflammatory Agents, Fatty Acids, Unsaturated, Humans, Inflammation, Models, Biological, Phospholipids, Dinoprostone, Cytokines, Inflammation Mediators
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