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父母 ω-3 脂肪酸摄入对后代微生物组和免疫的影响。

Effects of parental omega-3 fatty acid intake on offspring microbiome and immunity.

机构信息

Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.

出版信息

PLoS One. 2014 Jan 29;9(1):e87181. doi: 10.1371/journal.pone.0087181. eCollection 2014.

Abstract

The "Western diet" is characterized by increased intake of saturated and omega-6 (n-6) fatty acids with a relative reduction in omega-3 (n-3) consumption. These fatty acids can directly and indirectly modulate the gut microbiome, resulting in altered host immunity. Omega-3 fatty acids can also directly modulate immunity through alterations in the phospholipid membranes of immune cells, inhibition of n-6 induced inflammation, down-regulation of inflammatory transcription factors, and by serving as pre-cursors to anti-inflammatory lipid mediators such as resolvins and protectins. We have previously shown that consumption by breeder mice of diets high in saturated and n-6 fatty acids have inflammatory and immune-modulating effects on offspring that are at least partially driven by vertical transmission of altered gut microbiota. To determine if parental diets high in n-3 fatty acids could also affect offspring microbiome and immunity, we fed breeding mice an n-3-rich diet with 40% calories from fat and measured immune outcomes in their offspring. We found offspring from mice fed diets high in n-3 had altered gut microbiomes and modestly enhanced anti-inflammatory IL-10 from both colonic and splenic tissue. Omega-3 pups were protected during peanut oral allergy challenge with small but measurable alterations in peanut-related serologies. However, n-3 pups displayed a tendency toward worsened responses during E. coli sepsis and had significantly worse outcomes during Staphylococcus aureus skin infection. Our results indicate excess parental n-3 fatty acid intake alters microbiome and immune response in offspring.

摘要

“西方饮食”的特点是摄入更多的饱和脂肪和欧米伽-6(n-6)脂肪酸,而欧米伽-3(n-3)的摄入量相对减少。这些脂肪酸可以直接和间接调节肠道微生物群,导致宿主免疫改变。欧米伽-3 脂肪酸也可以通过改变免疫细胞的磷脂膜、抑制 n-6 诱导的炎症、下调炎症转录因子,以及作为抗炎脂质介质如 resolvins 和 protectins 的前体,直接调节免疫。我们之前已经表明,高饱和脂肪和 n-6 脂肪酸的饮食会对繁殖鼠的后代产生炎症和免疫调节作用,这些作用至少部分是由肠道微生物群的垂直传递改变所驱动的。为了确定高 n-3 脂肪酸的父母饮食是否也会影响后代的微生物群和免疫,我们用含有 40%脂肪热量的 n-3 丰富饮食喂养繁殖鼠,并测量其后代的免疫结果。我们发现,用富含 n-3 的饮食喂养的老鼠的后代肠道微生物群发生了改变,结肠和脾脏组织中的抗炎细胞因子 IL-10 也适度增强。花生口服过敏挑战中,n-3 后代的变化较小,但与花生相关的血清学发生了可测量的改变,得到了保护。然而,n-3 后代在大肠杆菌败血症期间的反应有恶化的趋势,在金黄色葡萄球菌皮肤感染期间的结果明显更差。我们的结果表明,过量的父母 n-3 脂肪酸摄入会改变后代的微生物群和免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78c4/3906117/5658dab0a235/pone.0087181.g001.jpg

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