Dietary ω-3 fatty acids and their influence on inflammation via Toll-like receptor pathways
Mahsa Jalili Nutrition Volume 85, May 2021, 111070
Highlights
• Long, highly unsaturated ω-3 fatty acids are considered indispensable for the human diet.
• The mechanism of action is based on lipid rafts, cytokines, and pathogen recognition receptors.
• Eicosapentaenoic acid and docosahexaenoic acid can modulate the nuclear factor-κB activation pathway.
• Lipopolysaccharide and Toll-like receptor-4 were the most studied signaling pathways in this topic.
• Further research is needed to investigate the role of plants in long-chain ω-3 fatty acids.
Dietary intake of long-chain, highly unsaturated ω-3 fatty acids (FAs) is considered indispensable for humans. The ω-3 FAs have been known to be anti-inflammatory and immunomodulatory dietary factors; however, the modes of action on pathogen recognition receptors (PRRs) and downstream signaling pathways have not been fully elucidated. Dietary sources contain various amounts of ω-3 long-chain fatty acids (LCFAs) of different lengths 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 modification of lipid rafts, 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 been implicated in the modulation of 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 nuclear factor-κB 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.