Department of Pathology, Section on Comparative Medicine, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157, USA.
College of Health and Medicine, School of Health Sciences, University of Tasmania, Launceston, TAS 7248, Australia.
Nutrients. 2022 Feb 25;14(5):977. doi: 10.3390/nu14050977.
Age-related alterations in the gut microbiome composition and its impacts on the host's health have been well-described; however, detailed analyses of the gut microbial structure defining ecological microbe-microbe interactions are limited. One of the ways to determine these interactions is by understanding microbial co-occurrence patterns. We previously showed promising abilities of DDS-1 on the aging gut microbiome and immune system. However, the potential of the DDS-1 strain to modulate microbial co-occurrence patterns is unknown. Hence, we aimed to investigate the ability of DDS-1 to modulate the fecal-, mucosal-, and cecal-related microbial co-occurrence networks in young and aging C57BL/6J mice. Our Kendall's tau correlation measures of co-occurrence revealed age-related changes in the gut microbiome, which were characterized by a reduced number of nodes and associations across sample types when compared to younger mice. After four-week supplementation, DDS-1 differentially modulated the overall microbial community structure in fecal and mucosal samples as compared to cecal samples. Beneficial bacteria such as and acted as connectors in aging networks in response to DDS-1 supplementation. Our findings provided the first evidence of the DDS-1-induced gut microbial ecological interactions, revealing the complex structure of microbial ecosystems with age.
年龄相关的肠道微生物群落组成的改变及其对宿主健康的影响已经得到了很好的描述；然而，详细分析定义生态微生物-微生物相互作用的肠道微生物结构仍然有限。确定这些相互作用的方法之一是了解微生物的共现模式。我们之前已经证明了 DDS-1 在衰老肠道微生物组和免疫系统方面的巨大潜力。然而，DDS-1 菌株调节微生物共现模式的潜力尚不清楚。因此，我们旨在研究 DDS-1 调节年轻和衰老 C57BL/6J 小鼠粪便、黏膜和盲肠相关微生物共现网络的能力。我们的 Kendall tau 共现测量揭示了肠道微生物组与年龄相关的变化，与年轻小鼠相比，粪便和黏膜样本中的节点和关联数量减少。经过四周的补充，与盲肠样本相比，DDS-1 对粪便和黏膜样本中的整体微生物群落结构产生了差异调节。有益细菌，如 和 ，作为响应 DDS-1 补充的衰老网络中的连接器。我们的研究结果首次提供了 DDS-1 诱导的肠道微生物生态相互作用的证据，揭示了随着年龄增长微生物生态系统的复杂结构。
