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