Key Laboratory of Food Nutrition and Functional Food of Hainan Province, School of Food Science and Engineering, Hainan University, Haikou, 570228, China.
School of Food Science and Technology, Jiangnan University, Wuxi, Jiangsu, China.
NPJ Biofilms Microbiomes. 2023 Oct 14;9(1):80. doi: 10.1038/s41522-023-00447-8.
Probiotics often acquire potentially adaptive mutations in vivo, gaining new functional traits through gut selection. While both the host and microbiome can contribute to probiotics' genetic evolution, separating the microbiome and the host's contribution to such selective pressures remains challenging. Here, we introduced germ-free (GF) and specific pathogen-free (SPF) mouse models to track how probiotic strains, i.e., Lactiplantibacillus plantarum HNU082 (Lp082) and Bifidobacterium animalis subsp. lactis V9 (BV9), genetically evolved under selection pressures derived from host factors alone and both host and microbial ecological factors. Notably, compared to the genome of a probiotic strain before consumption, the host only elicited <15 probiotic mutations in probiotic genomes that emerged in the luminal environment of GF mice, while a total of 840 mutations in Lp082 mutants and 21,579 mutations in BV9 were found in SPF mice, <0.25% of those derived from both factors that were never captured by other experimental evolution studies, indicating that keen microbial competitions exhibited the predominant evolutionary force in shaping probiotic genetic composition (>99.75%). For a given probiotic, functional genes occurring in potentially adaptive mutations induced by hosts (GF mice) were all shared with those found in mutants of SPF mice. Collectively, the native microbiome consistently drove a more rapid and divergent genetic evolution of probiotic strains in seven days of colonization than host factors did. Our study further laid a theoretical foundation for genetically engineering probiotics for better gut adaptation through in vitro artificial gut ecosystems without the selection pressures derived from host factors.
益生菌通常在体内获得潜在适应性突变,通过肠道选择获得新的功能特征。尽管宿主和微生物组都可以促进益生菌的遗传进化,但将微生物组和宿主对这些选择压力的贡献分开仍然具有挑战性。在这里,我们引入了无菌(GF)和特定病原体自由(SPF)小鼠模型,以跟踪益生菌菌株(即植物乳杆菌 HNU082(Lp082)和动物双歧杆菌亚种。 lactis V9(BV9))在仅由宿主因素和宿主和微生物生态因素共同产生的选择压力下遗传进化。值得注意的是,与益生菌菌株在消耗前的基因组相比,宿主仅在 GF 小鼠的腔环境中诱导益生菌基因组中出现的益生菌突变<15 个,而在 SPF 小鼠中,Lp082 突变体中总共发现了 840 个突变体和 BV9 中的 21579 个突变体<0.25%源自这两个因素,从未被其他实验进化研究捕获,表明激烈的微生物竞争表现出塑造益生菌遗传组成的主要进化力量(>99.75%)。对于给定的益生菌,由宿主(GF 小鼠)诱导的潜在适应性突变中出现的功能基因都与 SPF 小鼠突变体中发现的功能基因共享。总的来说,在定植的七天内,原生微生物组比宿主因素更能促进益生菌菌株的快速和不同的遗传进化。我们的研究进一步为通过体外人工肠道生态系统进行遗传工程益生菌以更好地适应肠道奠定了理论基础,而无需宿主因素带来的选择压力。