Dietary ω-3 fatty acids and their influence on inflammation via Toll-like receptor pathways

Mahsa Jalili*, Azita Hekmatdoost

*Corresponding author for this work

Research output: Contribution to journalReviewResearchpeer-review

23 Citations (Scopus)

Abstract

Dietary intake of long, highly unsaturated ω-3 fatty acids (FAs) is considered indispensable for humans. The ω-3 FAs have been known as anti-inflammatory and immunomodulatory dietary factors; however, the mode of action on pathogen recognition receptors (PRRs) and downstream signaling pathways were not elucidated completely. Dietary sources contain various amounts of ω-3 long chain fatty acids (LCFAs) of different length and the association between intake of these polyunsaturated fatty acids (PUFAs) with underlying mechanisms of various immune-related disorders can be of great interest. The potential anti-inflammatory role for ω-3 LCFAs can be explained by a- modification of lipid rafts, b- modulation of inflammatory mediators such as cytokines and PRRs. Toll-like receptors (TLRs) are a group of PRRs that play an important role in the recognition of bacterial infections and ω-3 FAs have for example been implicated to modulate downstream signaling of TLR-4, an important receptor for recognition of gram-negative bacteria. The ω-3 FAs docosahexaenoic acid and eicosapentaenoic acid have been investigated in vivo and in vitro for their effects on the neuclear factor-κβ activation pathway. Identification of the effects of ω-3 FAs on other key molecular factors like prostaglandins and leukotrienes and their signals may help the recognition and development of medicines to suppress the main mediators and turn on the expression of anti-inflammatory cytokines and nuclear receptors.
Original languageEnglish
Article number111070
JournalNutrition
Volume85
Number of pages10
ISSN0899-9007
DOIs
Publication statusPublished - 2021
Externally publishedYes

Keywords

  • Faculty of Science
  • Eicosapentaenoic acid
  • Docosahexaenoic acid
  • Toll-like receptors
  • Innate immunity

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