Xie Shuo, Ma Junze, Lu Zheng
Hainan Province Key Laboratory of One Health, Collaborative Innovation Center of One Health, School of Life and Health Sciences, Hainan University, Haikou, Hainan, China.
Guangdong Provincial Key Laboratory of Marine Biotechnology, Department of Biology, Institute of Marine Sciences, Shantou University, Shantou, China.
Front Microbiol. 2024 Dec 11;15:1505218. doi: 10.3389/fmicb.2024.1505218. eCollection 2024.
This study probes into the unique metabolic responses of (), a key player in the gut microbiota, when it metabolizes rhamnose rather than typical carbohydrates. Known for its predominant role in the Bacteroidetes phylum, efficiently breaks down poly- and mono-saccharides into beneficial short-chain fatty acids (SCFAs), crucial for both host health and microbial ecology balance. Our research focused on how this bacterium's SCFA production differ when utilizing various monosaccharides, with an emphasis on the oxidative stress responses triggered by rhamnose consumption. Notably, rhamnose use results in unique metabolic byproducts, including substantial quantities of 1,2-propanediol, which differs significantly from those produced during glucose metabolism. Our research reveals that rhamnose consumption is associated with a reduction in reactive oxygen species (ROS), signifying improved resistance to oxidative stress compared to other sugars. This effect is attributed to specific gene expressions within the rhamnose metabolic pathway. Notably, overexpression of the rhamnose metabolism regulator RhaR in enhances its survival in oxygen-rich conditions by reducing hydrogen peroxide production. This reduction is linked to decreased expression of pyruvate:ferredoxin oxidoreductase (PFOR). In contrast, experiments with a -deficient strain demonstrated that the absence of RhaR causes cells growing on rhamnose to produce ROS at rates comparable to cells grown on glucose, therefore, losing their advantage in oxidative resistance. Concurrently, the expression of PFOR is no longer suppressed. These results indicate that when is cultured in a rhamnose-based medium, RhaR can restrain the expression of PFOR. Although PFOR is not a primary contributor to intracellular ROS production, its sufficient inhibition does reduce ROS levels to certain extent, consequently improving the bacterium's resistance to oxidative stress. It highlights the metabolic flexibility and robustness of microbes in handling diverse metabolic challenges and oxidative stress in gut niches through the consumption of alternative carbohydrates.
本研究探究了肠道微生物群中的关键成员（）在代谢鼠李糖而非典型碳水化合物时的独特代谢反应。因其在拟杆菌门中占主导地位而闻名，它能有效地将多糖和单糖分解为有益的短链脂肪酸（SCFAs），这对宿主健康和微生物生态平衡都至关重要。我们的研究聚焦于这种细菌在利用各种单糖时产生短链脂肪酸的差异，重点关注鼠李糖消耗引发的氧化应激反应。值得注意的是，利用鼠李糖会产生独特的代谢副产物，包括大量的1,2 - 丙二醇，这与葡萄糖代谢过程中产生的副产物有显著差异。我们的研究表明，消耗鼠李糖与活性氧（ROS）的减少有关，这意味着与其他糖类相比，其对氧化应激的抵抗力有所提高。这种效应归因于鼠李糖代谢途径中的特定基因表达。值得注意的是，在中过表达鼠李糖代谢调节因子RhaR可通过减少过氧化氢的产生来提高其在富氧条件下的存活率。这种减少与丙酮酸：铁氧还蛋白氧化还原酶（PFOR）的表达降低有关。相反，对缺陷菌株的实验表明，缺乏RhaR会导致在鼠李糖上生长的细胞产生ROS的速率与在葡萄糖上生长的细胞相当，因此失去了它们在抗氧化方面的优势。同时，PFOR的表达不再受到抑制。这些结果表明，当在以鼠李糖为基础的培养基中培养时，RhaR可以抑制PFOR的表达。虽然PFOR不是细胞内ROS产生的主要贡献者，但其充分抑制确实在一定程度上降低了ROS水平，从而提高了细菌对氧化应激的抵抗力。它凸显了微生物通过消耗替代碳水化合物在应对肠道生态位中各种代谢挑战和氧化应激方面的代谢灵活性和稳健性。
