PDF(Pubmed)
Abstract：
The microbiota significantly impacts digestive epithelium functionality, especially in nutrient processing. Given the importance of iron for both the host and the microbiota, we hypothesized that host-microbiota interactions fluctuate with dietary iron levels. We compared germ-free (GF) and conventional mice (SPF) fed iron-containing (65 mg/Kg) or iron-depleted (<6 mg/Kg) diets. The efficacy of iron privation was validated by iron blood parameters. Ferritin and Dmt1, which represent cellular iron storage and transport respectively, were studied in tissues where they are abundant: the duodenum, liver and lung. When the mice were fed an iron-rich diet, the microbiota increased blood hemoglobin and hepcidin and the intestinal ferritin levels, suggesting that the microbiota helps iron storage. When iron was limiting, the microbiota inhibited the expression of the intestinal Dmt1 transporter, likely via the pathway triggered by Hif-2α. The microbiota assists the host in storing intestinal iron when it is abundant and competes with the host by inhibiting Dmt1 in conditions of iron scarcity. Comparison between duodenum, liver and lung indicates organ-specific responses to microbiota and iron availability. Iron depletion induced temporal changes in microbiota composition and activity, reduced α-diversity of microbiota, and led to Lactobacillaceae becoming particularly more abundant after 60 days of privation. By inoculating GF mice with a simplified bacterial mixture, we show that the iron-depleted host favors the gut fitness of Bifidobacterium longum.
摘要：
微生物群显著影响消化上皮功能，尤其是在营养加工中。鉴于铁对宿主和微生物群的重要性，我们假设宿主-微生物群相互作用随饮食铁水平而波动.我们比较了饲喂含铁（65mg/Kg）或铁耗尽（<6mg/Kg）饮食的无菌（GF）和常规小鼠（SPF）。通过铁血参数验证了铁剥夺的功效。铁蛋白和Dmt1分别代表细胞铁的储存和运输，在它们丰富的组织中进行了研究：十二指肠，肝和肺。当老鼠吃富含铁的食物时，微生物群增加了血液血红蛋白和铁调素以及肠道铁蛋白水平，这表明微生物有助于铁的储存。当铁限制时，微生物群抑制肠道Dmt1转运蛋白的表达，可能是通过Hif-2α触发的途径。当微生物群丰富时，微生物群协助宿主储存肠道铁，并在铁缺乏的条件下通过抑制Dmt1与宿主竞争。十二指肠之间的比较，肝和肺表明器官对微生物群和铁可用性的特异性反应。铁耗竭引起的微生物群组成和活性的时间变化，减少微生物群的α-多样性，并导致乳杆菌科在剥夺60天后变得特别丰富。通过用简化的细菌混合物接种GF小鼠，我们表明，铁耗尽的宿主有利于长双歧杆菌的肠道适应性。
