Iron Modulates Butyrate Production by a Child Gut Microbiota In Vitro.
Iron Modulates Butyrate Production by a Child Gut Microbiota In Vitro.
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DOI：
10.1128/mbio.01453-15
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发表时间：
2015-11-17
期刊：
影响因子：
6.4
通讯作者：
Chassard C
中科院分区：
文献类型：
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作者：
Dostal A;Lacroix C;Bircher L;Pham VT;Follador R;Zimmermann MB;Chassard C
本研究的目的是调查铁 (Fe) 可用性对人类肠道复杂细菌生态系统中丁酸盐生成的影响。因此，在接种了来自儿童的固定肠道微生物群的体外结肠发酵模型（称为 PolyFermS 的聚合发酵肠模型）和丁酸盐生产者 Roseburia Enteris 的分批培养物中模拟了不同的铁利用率。评估了微生物群落的变化（16S rRNA 测序和定量 PCR）、代谢活动（高效液相色谱）以及参与丁酸生产的基因表达。在PolyFermS中，与正常Fe条件下的结果相比，中度Fe缺乏导致丁酸产量增加1.4倍，丁酰辅酶A（CoA）：乙酸CoA转移酶基因表达增加5倍，而非常强烈的Fe缺乏则显着降低丁酸浓度和丁酸产生细菌。在低铁环境中生长的 R. intestinalis 的分批培养物优先产生乳酸，并减少丁酸和氢气的产生，同时乳酸脱氢酶基因上调和丙酮酸：铁氧还蛋白氧化还原酶基因下调。相反，与正常铁条件下的结果相比，在高铁条件下，R. intestinalis 培养物显示出丁酸盐和氢气产量增加，以及相应基因的表达增加。我们的数据揭示了铁对肠道微生物丁酸生产者和丁酸浓度的强烈调节作用，这有助于维持宿主肠道健康。缺铁是全世界最常见的营养缺乏症之一，可以通过补充铁来纠正。在这项体外研究中，我们表明，在密切模仿儿童肠道微生物群的连续肠道发酵模型中，环境铁浓度强烈影响肠道微生物组的组成及其代谢活动，特别是丁酸盐的产生。不同Fe条件下参与丁酸生产途径的基因的差异表达以及Fe的酶辅因子作用解释了观察到的丁酸生产的调节。我们的数据表明，到达结肠的膳食铁水平会影响微生物组及其为宿主提供有益丁酸盐的基本功能。
The aim of this study was to investigate the effect of iron (Fe) availability on butyrate production in the complex bacterial ecosystem of the human gut. Hence, different Fe availabilities were mimicked in an in vitro colonic fermentation model (the polyfermenter intestinal model called PolyFermS) inoculated with immobilized gut microbiota from a child and in batch cultures of the butyrate producer Roseburia intestinalis. Shifts in the microbial community (16S rRNA sequencing and quantitative PCR), metabolic activity (high-performance liquid chromatography), and expression of genes involved in butyrate production were assessed. In the PolyFermS, moderate Fe deficiency resulted in a 1.4-fold increase in butyrate production and a 5-fold increase in butyryl-coenzyme A (CoA):acetate CoA-transferase gene expression, while very strong Fe deficiency significantly decreased butyrate concentrations and butyrate-producing bacteria compared with the results under normal Fe conditions. Batch cultures of R. intestinalis grown in a low-Fe environment preferentially produced lactate and had reduced butyrate and hydrogen production, in parallel with upregulation of the lactate dehydrogenase gene and downregulation of the pyruvate:ferredoxin-oxidoreductase gene. In contrast, under high-Fe conditions, R. intestinalis cultures showed enhanced butyrate and hydrogen production, along with increased expression of the corresponding genes, compared with the results under normal-Fe conditions. Our data reveal the strong regulatory effect of Fe on gut microbiota butyrate producers and on the concentrations of butyrate, which contributes to the maintenance of host gut health. Fe deficiency is one of the most common nutritional deficiencies worldwide and can be corrected by Fe supplementation. In this in vitro study, we show that environmental Fe concentrations in a continuous gut fermentation model closely mimicking a child’s gut microbiota strongly affect the composition of the gut microbiome and its metabolic activity, particularly butyrate production. The differential expression of genes involved in the butyrate production pathway under different Fe conditions and the enzyme cofactor role of Fe explain the observed modulation of butyrate production. Our data reveal that the level of dietary Fe reaching the colon affects the microbiome, and its essential function of providing the host with beneficial butyrate.