Frontiers in microbiomes最新文献

The macronutrient composition of a host's diet shapes its gut microbial community, with dietary fiber in particular escaping host digestion to serve as a potent carbon source for gut microbiota. Despite widespread recognition of fiber's importance to microbiome health, nutritional research often fails to differentiate hyper-processed fibers from cell-matrix-derived intrinsic fibers, limiting our understanding of how individual polysaccharides influence the gut community. We use the American cockroach (Periplaneta americana) as a model system to dissect the response of complex gut microbial communities to dietary modifications that are difficult to test in traditional host models. Here, we designed synthetic diets from lab-grade, purified ingredients to identify how the cockroach microbiome responds to six different carbohydrates (chitin, methylcellulose, microcrystalline cellulose, pectin, starch, and xylan) in otherwise balanced diets. We show via 16S rRNA gene profiling that these synthetic diets reduce bacterial diversity and alter the phylogenetic composition of cockroach gut microbiota in a fiber-dependent manner, regardless of the vitamin and protein content of the diet. Comparisons with cockroaches fed whole-food diets reveal that synthetic diets induce blooms in common cockroach-associated taxa and subsequently fragment previously stable microbial correlation networks. Our research leverages an unconventional microbiome model system and customizable lab-grade artificial diets to shed light on how purified polysaccharides, as opposed to nutritionally complex intrinsic fibers, exert substantial influence over a normally stable gut community.

Chronic Obstructive Pulmonary Disease (COPD) affects 30 million Americans. Previous epidemiologic work has shown that diet can impact pulmonary function in those with and without COPD. Diet is also a major driver of gut microbiome composition and function. Importantly, the gut microbiome has also been associated with lung health (i.e., the gut-lung axis) in both preclinical and clinical studies. Despite this growing body of evidence, many questions remain regarding the gut-lung axis. Specifically, how the microbiome impacts the relationship between diet factors and spirometry or stage of disease in people with COPD is little understood. We hypothesize that there are taxonomic differences in the gut microbiome among the different stages of COPD and that diet microbiome interactions influence pulmonary function. This study aimed to identify how the GI microbiota correlated with the severity of respiratory disease in COPD patients and how the microbiome may mediate the relationship between diet, including fiber and omega-3 fatty acids, and lung function outcomes.

Type 2 diabetes (T2D) is a common forerunner of neurodegeneration and accompanying dementia, including Alzheimer's Disease (AD), yet the mechanisms underlying this comorbidity remain unresolved. Individuals of Mexican descent living in South Texas have increased prevalence of comorbid T2D and early onset AD, despite low incidence of the APOE-ε4 risk variant among the population and an absence of a similar predisposition among relatives residing in Mexico - suggesting a role for environmental factors in coincident T2D and AD susceptibility. We therefore sought to test if differences in gut community structure could be observed in this population prior to any AD diagnosis. Here, in a small clinical trial (ClinicalTrials.gov Identifier NCT04602650), we report evidence for altered gut microbial ecology among subjects of Mexican descent living in South Texas with T2D (sT2D) compared to healthy controls without T2D (HC), despite no differences in expressed dietary preferences. We performed metataxonomic 16S rRNA gene amplicon sequencing of study participant stool samples. Although no significant decrease in microbial alpha diversity was observed between sT2D gut communities versus those of HC, body mass index was identified as a driver of gut community structure. Intriguingly, we observed a significant negative association of Faecalibacterium with T2D and an increase in the abundance of pathobionts Escherichia-Shigella, Enterobacter, and the erysipelotrichial species Clostridia innocuum among sT2D gut microbiota, as well as differentially abundant gene and metabolic pathways. Future large-scale, longitudinal sequencing efforts of the gut microbiome of individuals with T2D who go onto develop AD might identify key actors among "disease state" microbiota that contribute to increased susceptibility to comorbid dementia among type 2 diabetics. Finally, we identified candidate microbiome-targeted approaches for the treatment of T2D.