Western Human Nutrition Research Center, ARS, USDA and Department of Nutrition, University of California, Davis, CA, USA.
Nutr Rev. 2010 Jan;68(1):38-61. doi: 10.1111/j.1753-4887.2009.00259.x.
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.
慢性炎症被认为会促进许多慢性疾病的发展。模式识别受体（PRRs）、Toll 样受体（TLRs）和核苷酸结合寡聚化结构域蛋白（NODs）分别通过识别病原体相关分子模式和内源性分子来介导感染诱导的炎症和无菌性炎症。PRR 介导的炎症是改变许多慢性疾病风险的重要决定因素。饱和脂肪酸（SFAs）可以激活 PRRs，导致促炎靶基因产物的表达增强。然而，n-3 多不饱和脂肪酸（PUFAs）抑制激动剂诱导的 PRR 激活。这些结果表明，SFAs 和 n-3 PUFAs 可以相互调节 PRR 介导的炎症，PRRs 及其下游信号成分是饮食策略的分子靶点，可减少慢性炎症和随后发生慢性疾病的风险。这一知识的进步为理解不同膳食脂肪酸如何改变包括胰岛素抵抗、动脉粥样硬化和癌症在内的慢性疾病风险的机制提供了一个新的范例。
