Modulation of pattern recognition receptor-mediated inflammation and risk of chronic diseases by dietary fatty acids.

Abstract

Chronic inflammation is known to promote the development of many chronic diseases. Pattern recognition receptors (PRRs), Toll-like receptors (TLRs), and nucleotide-binding oligomerization domain proteins (NODs) mediate both infection-induced inflammation and sterile inflammation by recognizing pathogen- associated molecular patterns and endogenous molecules, respectively. PRR-mediated inflammation is an important determinant in altering the risk of many chronic diseases. Saturated fatty acids (SFAs) can activate PRRs, leading to enhanced expression of pro-inflammatory target gene products. However, n-3 polyunsaturated fatty acids (PUFAs) inhibit agonist-induced activation of PRRs. These results suggest that SFAs and n-3 PUFAs can reciprocally modulate PRR-mediated inflammation, and that PRRs and their downstream signaling components are molecular targets for dietary strategies to reduce chronic inflammation and subsequent risk of chronic diseases. This advancement in knowledge provides a new paradigm for understanding the mechanism by which different dietary fatty acids modify risk of chronic diseases including insulin resistance, atherosclerosis, and cancer.

• Authors: Joo Y Lee, Ling Zhao, Daniel H Hwang
• Journal: Nutrition reviews (Nutr Rev) Vol. 68 Issue 1 Pg. 38-61 (Jan 2010) ISSN: 1753-4887 [Electronic] United States
• PMID: 20041999 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S., Review)

Chemical References

• Dietary Fats
• Fatty Acids
• Fatty Acids, Omega-3
• Nod Signaling Adaptor Proteins
• Receptors, Pattern Recognition
• Toll-Like Receptors

Topics

• Animals
• Chronic Disease (prevention & control)
• Dietary Fats
• Fatty Acids (metabolism, physiology)
• Fatty Acids, Omega-3 (metabolism, physiology)
• Humans
• Inflammation (physiopathology)
• Nod Signaling Adaptor Proteins (agonists, antagonists & inhibitors, physiology)
• Receptors, Pattern Recognition (agonists, antagonists & inhibitors, physiology)
• Risk Factors
• Toll-Like Receptors (agonists, antagonists & inhibitors, physiology)