Background: There is general consensus that consumption of dietary fermentable fiber improves cardiometabolic health, in part by promoting mutualistic microbes and by increasing production of beneficial metabolites in the distal gut. However, human studies have reported variations in the observed benefits among individuals consuming the same fiber. Several factors likely contribute to this variation, including host genetic and gut microbial differences. We hypothesized that gut microbial metabolism of dietary fiber represents an important and differential factor that modulates how dietary fiber impacts the host.Results: We examined genetically identical gnotobiotic mice harboring two distinct complex gut microbial communities and exposed to four isocaloric diets, each containing different fibers: (i) cellulose, (ii) inulin, (iii) pectin, (iv) a mix of 5 fermentable fibers (assorted fiber). Gut microbiome analysis showed that each transplanted community preserved a core of common taxa across diets that differentiated it from the other community, but there were variations in richness and bacterial taxa abundance within each community among the different diet treatments. Host epigenetic, transcriptional, and metabolomic analyses revealed diet-directed differences between animals colonized with the two communities, including variation in amino acids and lipid pathways that were associated with divergent health outcomes.Conclusion: This study demonstrates that interindividual variation in the gut microbiome is causally linked to differential effects of dietary fiber on host metabolic phenotypes and suggests that a one-fits-all fiber supplementation approach to promote health is unlikely to elicit consistent effects across individuals. Overall, the presented results underscore the importance of microbe-diet interactions on host metabolism and suggest that gut microbes modulate dietary fiber efficacy.

We evaluated associations of smoking heaviness markers and the effects of smoking cessation on the intestinal microbiota and cardiovascular disease risk factors in current smokers undertaking a quit attempt. Participants were current smokers enrolled in a prospective randomized clinical trial of smoking cessation therapies with visits at baseline, 2, and 12 weeks. Genomic DNA was extracted from fecal samples followed by 16S rRNA gene sequencing and analysis using the QIIME2 software workflow. Relative abundances of bacterial taxa and alpha- and beta-diversity measures were used for comparisons. The 36 smokers were (mean (standard deviation)) 51.5 (11.1) years old (42% male) and smoked 15.1 (6.4) cigarettes per day for 22.7 (11.9) pack-years. Relative abundances of the phylum Actinobacteria correlated with pack-years (rho = −0.44, p = 0.008) and Cyanobacteria correlated with CO levels (rho = 0.39, p = 0.021). After 12 weeks, relative abundances of the phylum Bacteroidetes increased (p_ANCOVA = 0.048) and Firmicutes decreased (p_ANCOVA = 0.036) among abstainers compared to continuing smokers. Increases in alpha-diversity were associated with heart rates (rho = −0.59, p = 0.037), systolic blood pressures (rho = −0.58, p = 0.043), and C-reactive protein (rho = −0.60, p = 0.034). Smoking cessation led to minor changes in the intestinal microbiota. It is unclear if the proven health benefits of smoking cessation lead to salutary changes in the intestinal microbiota.

Chronic wounds are a common and costly complication of diabetes, where multifactorial defects contribute to dysregulated skin repair, inflammation, tissue damage, and infection. We previously showed that aspects of the diabetic foot ulcer microbiota were correlated with poor healing outcomes, but many microbial species recovered remain uninvestigated with respect to wound healing. Here, we focused on Alcaligenes faecalis , a Gram-negative bacterium that is frequently recovered from chronic wounds but rarely causes infection. Treatment of diabetic wounds with A. faecalis accelerated healing during early stages. We investigated the underlying mechanisms and found that A. faecalis treatment promotes reepithelialization of diabetic keratinocytes, a process that is necessary for healing but deficient in chronic wounds. Overexpression of matrix metalloproteinases in diabetes contributes to failed epithelialization, and we found that A. faecalis treatment balances this overexpression to allow proper healing. This work uncovers a mechanism of bacterial-driven wound repair and provides a foundation for the development of microbiota-based wound interventions.

Gut microbiota is associated with the development of metabolic disorders. To study its association with childhood obesity, we performed a cross-sectional study with 46 children (6–12 years old). We collected fecal samples, food-frequency questionnaires (FFQs), and anthropometric measurements. Shotgun metagenomics were used to obtain the microbial taxonomic diversity and metabolic potential. We identified two dietary profiles characterized by complex carbohydrates and proteins (pattern 1) and saturated fat and simple carbohydrates (pattern 2). We classified each participant into normal weight (NW) or overweight and obese (OWOB) using their body mass index (BMI) z-score. The ratio of Firmicutes/Bacteroidetes and alpha diversity were not different between the BMI groups. Genera contributing to beta diversity between NW and OWOB groups included Bacteroides rodentium, B. intestinalis, B. eggerthii, Methanobrevibacter smithii, Eubacterium sp., and Roseburia sp. B. rodentium was associated with lower BMI and dietary pattern 1 intake. Eubacterium sp. and Roseburia sp. were associated with BMI increments and high consumption of dietary pattern 2. Methane and energy metabolism were found enriched in under-represented KEGG pathways of NW group compared to OWOB. Complex dietary and microbiome interaction leads to metabolic differences during childhood, which should be elucidated to prevent metabolic diseases in adolescence and adulthood.

The alteration of gut microbiome composition has been commonly observed in diseases involving inflammation, such as obesity and metabolic impairment. Inflammatory host response in the gut can be a consequence of dietary driven dysbiosis.