The gut microbiota has been identified as a target of toxic metals and a potentially crucial mediator of the bioavailability and toxicity of these metals. In this study, we show that aluminum (Al) exposure, even at low dose, affected the growth of representative strains from the human intestine via pure culture experiments. In vitro, Lactobacillus plantarum CCFM639 could bind Al on its cell surface as shown by electron microscopy and energy dispersive X-ray analysis. The potential of L. plantarum CCFM639 to reverse changes in human intestine microbiota induced by low-dose dietary Al exposure was investigated using an in vitro colonic fermentation model. Batch fermenters were inoculated with fresh stool samples from healthy adult donors and supplemented with 86 mg/L Al and/or 10⁹ CFU of L. plantarum CCFM639. Al exposure significantly increased the relative abundances of Bacteroidetes (Prevotella), Proteobacteria (Escherichia), Actinobacteria (Collinsella), Euryarchaeota (Methanobrevibacter), and Verrucomicrobiaceae and decreased Firmicutes (Streptococcus, Roseburia, Ruminococcus, Dialister, Coprobacillus). Some changes were reversed by the inclusion of L. plantarum CCFM639. Alterations in gut microbiota induced by Al and L. plantarum CCFM639 inevitably led to changes in metabolite levels. The short-chain fatty acid (SCFAs) contents were reduced after Al exposure, but L. plantarum CCFM639 could elevate their levels. SCFAs had positive correlations with beneficial bacteria, such as Dialister, Streptococcus, Roseburia, and negative correlations with Erwinia, Escherichia, and Serratia. Therefore, dietary Al exposure altered the composition and structure of the human gut microbiota, and this was partially mitigated by L. plantarum CCFM639. This probiotic supplementation is potentially a promising and safe approach to alleviate the harmful effects of dietary Al exposure.

肠道微生物群已被确定为有毒金属的目标，也是这些金属生物利用度和毒性的潜在关键介质。在这项研究中，我们通过纯培养实验表明，即使在低剂量下，铝 (Al) 暴露也会影响来自人类肠道的代表性菌株的生长。在体外，如电子显微镜和能量色散 X 射线分析所示，植物乳杆菌CCFM639 可以在其细胞表面结合 Al。使用体外结肠发酵模型研究了植物乳杆菌CCFM639 逆转由低剂量膳食铝暴露引起的人类肠道微生物群变化的潜力。用来自健康成人捐赠者的新鲜粪便样本接种分批发酵罐，并补充 86 mg/L Al 和/或 10⁹  CFU 的植物乳杆菌CCFM639。人曝光显著增加拟杆菌（的相对丰度普雷沃），变形菌（大肠杆菌），放线菌（柯林斯），广古菌门（甲烷短），和Verrucomicrobiaceae和降低厚壁菌门（链球菌，罗斯氏，瘤胃球菌属，Dialister，Coprobacillus）。加入植物乳杆菌CCFM639逆转了一些变化。铝和植物乳杆菌引起的肠道微生物群的改变CCFM639 不可避免地导致代谢物水平的变化。短链脂肪酸 (SCFA) 含量在铝暴露后降低，但植物乳杆菌CCFM639 可以提高其含量。SCFAs与Dialister、链球菌、Roseburia等有益菌呈正相关，与欧文氏菌、埃希氏菌、沙雷氏菌呈负相关。因此，膳食铝暴露改变了人类肠道微生物群的组成和结构，而植物乳杆菌可以部分缓解这种情况CCFM639。这种益生菌补充剂可能是一种有前景且安全的方法，可以减轻膳食铝暴露的有害影响。