The oral delivery of compounds associated with diet or medication have an impact on the gut microbiota balance, which in turn, influences the physiologic process. Several reports have shown significant advances in clarifying the impact, interactions and outcomes of oral intake of nanoparticles and the human gut. These interactions may affect the bioavailability of the delivered compounds. In addition, there is a considerable breakthrough in the development of antimicrobial nanoparticles for intestinal pathogenic bacteria. Several in vitro fermentation and in vivo models have been developed throughout the years and were used to test these systems. The methodologies and studies carried out so far on the modulation of human and animal gut microbiome by oral delivery nanosized materials were reviewed. Overall, the available in vitro studies mimic the real physiological events enabling to select the best production conditions of nanoparticulate systems in a preliminary stage of research. On the other hand, animal studies can be used to access the dosage effect, safety and correlation between haematological, biochemical and symptoms, with gut microbiota groups and metabolites.

Metabolites produced by microbial fermentation in the human intestine, especially short-chain fatty acids (SCFAs), are known to play important roles in colonic and systemic health. Our aim here was to advance our understanding of how and why their concentrations and proportions vary between individuals. We have analysed faecal concentrations of microbial fermentation acids from 10 human volunteer studies, involving 163 subjects, conducted at the Rowett Institute, Aberdeen, UK over a 7-year period. In baseline samples, the % butyrate was significantly higher, whilst % iso-butyrate and % iso-valerate were significantly lower, with increasing total SCFA concentration. The decreasing proportions of iso-butyrate and iso-valerate, derived from amino acid fermentation, suggest that fibre intake was mainly responsible for increased SCFA concentrations. We propose that the increase in % butyrate among faecal SCFA is largely driven by a decrease in colonic pH resulting from higher SCFA concentrations. Consistent with this, both total SCFA and % butyrate increased significantly with decreasing pH across five studies for which faecal pH measurements were available. Colonic pH influences butyrate production through altering the stoichiometry of butyrate formation by butyrate-producing species, resulting in increased acetate uptake and butyrate formation, and facilitating increased relative abundance of butyrate-producing species (notably Roseburia and Eubacterium rectale).

The human large intestinal microbiota thrives on dietary carbohydrates that are converted to a range of fermentation products. Short-chain fatty acids (acetate, propionate and butyrate) are the dominant fermentation acids that accumulate to high concentrations in the colon and they have health-promoting effects on the host. Although many gut microbes can also produce lactate, it usually does not accumulate in the healthy gut lumen. This appears largely to be due to the presence of a relatively small number of gut microbes that can utilise lactate and convert it to propionate, butyrate or acetate. There is increasing evidence that these microbes play important roles in maintaining a healthy gut environment. In this review, we will provide an overview of the different microbes involved in lactate metabolism within the gut microbiota, including biochemical pathways utilised and their underlying energetics, as well as regulation of the corresponding genes. We will further discuss the potential consequences of perturbation of the microbiota leading to lactate accumulation in the gut and associated disease states and how lactate-utilising bacteria may be employed to treat such diseases.

We investigated the impact of dried chicory root in a randomised, placebo-controlled trial with 55 subjects at risk for type 2 diabetes on bowel function, gut microbiota and its products, and glucose homeostasis. The treatment increased stool softness (+1.1 ± 0.3 units; p = 0.034) and frequency (+0.6 ± 0.2 defecations/day; p < 0.001), strongly modulated gut microbiota composition (7 % variation; p = 0.001), and dramatically increased relative levels (3-4-fold) of Anaerostipes and Bifidobacterium spp., in a dose-dependent, reversible manner. A synthetic community, including selected members of these genera and a Bacteroides strain, generated a butyrogenic trophic chain from the product. Faecal acetate, propionate and butyrate increased by 25.8 % (+13.0 ± 6.3 mmol/kg; p = 0.023) as did their fasting circulating levels by 15.7 % (+7.7 ± 3.9 μM; p = 0.057). In the treatment group the glycaemic coefficient of variation decreased from 21.3 ± 0.94 to 18.3 ± 0.84 % (p = 0.004), whereas fasting glucose and HOMA-ir decreased in subjects with low baseline Blautia levels (−0.3 ± 0.1 mmol/L fasting glucose; p = 0.0187; −0.14 ± 0.1 HOMA-ir; p = 0.045). Dried chicory root intake rapidly and reversibly affects bowel function, benefits butyrogenic trophic chains, and promotes glycaemic control.

Consumption of high-energy-yielding diets, rich in fructose and lipids, is a factor contributing to the current increase in non-alcoholic fatty liver disease prevalence. Gut microbiota composition and short-chain fatty acids (SCFAs) production alterations derived from unhealthy diets are considered putative underlying mechanisms. This study aimed to determine relationships between changes in gut microbiota composition and SCFA levels by comparing rats featuring diet-induced steatohepatitis with control counterparts fed a standard diet. A high-fat high-fructose (HFHF) feeding induced higher body, liver and mesenteric adipose tissue weights, increased liver triglyceride content and serum transaminase, glucose, non-HDL-c and MCP-1 levels. Greater liver malondialdehyde levels and glutathione peroxidase activity were also observed after feeding the hypercaloric diet. Regarding gut microbiota composition, a lowered diversity and increased abundances of bacteria from the Clostridium sensu stricto 1, Blautia, Eubacterium coprostanoligenes group, Flavonifractor, and UBA1819 genera were found in rats featuring diet-induced steatohepatitis, as well as higher isobutyric, valeric and isovaleric acids concentrations. These results suggest that hepatic alterations produced by a hypercaloric HFHF diet may be related to changes in overall gut microbiota composition and abundance of specific bacteria. The shift in SCFA levels produced by this unbalanced diet cannot be discarded as potential mediators of the reported hepatic and metabolic alterations.

Despite extensive research into the toxicology of the herbicide glyphosate, there are still major unknowns regarding its effects on the human gut microbiome. We describe the effects of glyphosate and a Roundup glyphosate-based herbicide on infant gut microbiota using SHIME technology. SHIME microbiota culture was undertaken in the presence of a concentration of 100-mg/L glyphosate and the same glyphosate equivalent concentration of Roundup. Roundup and to a lesser extent glyphosate caused an increase in fermentation activity, resulting in acidification of the microbial environment. This was also reflected by an increase in lactate and acetate production concomitant to a decrease in the levels of propionate, valerate, caproate and butyrate. Ammonium production reflecting proteolytic activities was increased by Roundup exposure. Global metabolomics revealed large-scale disturbances, including an increased abundance of long-chain polyunsaturated fatty acids. Changes in bacterial composition measured by qPCR and 16S rRNA suggested that lactobacilli had their growth stimulated as a result of microenvironment acidification. Co-treatment with the spore-based probiotic formulation MegaSporeBiotic reverted some of the changes in short-chain fatty acid levels. Altogether, our results suggest that glyphosate can exert effects on human gut microbiota.

Irritable bowel syndrome (IBS) is a disorder of gut–brain interaction with a complex pathophysiology. Growing evidence suggests that alterations of the gut microenvironment, including microbiota composition and function, may be involved in symptom generation. Therefore, attempts to modulate the gut microenvironment have provided promising results as an indirect approach for IBS management. Antibiotics, probiotics, prebiotics, food and faecal microbiota transplantation are the main strategies for alleviating IBS symptom severity by modulating gut microbiota composition and function (eg. metabolism), gut barrier integrity and immune activity, although with varying efficacy. In this narrative review, we aim to provide an overview of the current approaches targeting the gut microenvironment in order to indirectly manage IBS symptoms.

Acute appendicitis is a common acute surgical emergency; however, the pathogenesis of adult appendicitis remains poorly understood. The microbiome is increasingly thought to play a key role in inflammatory disease of the bowel and similarly, may play a role in appendicitis. This study aimed to characterise the microbiome of adult acute appendicitis in a prospective cohort. We recruited 60 adults with acute appendicitis and 20 healthy controls. Rectal swabs were taken from each patient. After DNA extraction, 16S rRNA amplicon sequencing was carried out for analysis of diversity and taxonomic abundance. Phylogenetic sequencing of the samples indicated that there is a difference between the microbial composition of those with acute appendicitis and healthy controls, with a statistically significant decrease in alpha diversity in rectal swabs of appendicitis patients compared to healthy controls. At the genus level, we saw an increased abundance of potential pathogens, for example, Parvimonas and Acinetobacter, and a decrease in commensal taxa such as Faecalibacterium, Blautia and Lachnospiraceae in appendicitis patients compared to healthy controls. There was a reduction in diversity and loss of commensals in the microbiome of those with acute appendicitis, which may play a role in the cascade leading to acute appendicitis or the result of this.

Human milk oligosaccharides (HMOs) are a class of structurally diverse and complex unconjugated glycans present in breast milk, which act as selective substrates for several genera of select microbes and inhibit the colonisation of pathogenic bacteria. Yet, not all infants are breastfed, instead being fed with formula milks which may or may not contain HMOs. Currently, formula milks only possess two HMOs: 2′-fucosyllactose (2’FL) and lacto-N-neotetraose (LNnT), which have been suggested to be similarly effective as human breast milk in supporting age-related growth. However, the in vivo evidence regarding their ability to beneficially reduce respiratory infections along with altering the composition of an infant’s microbiota is limited at best. Thus, this review will explore the concept of HMOs and their metabolic fate, and summarise previous in vitro and in vivo clinical data regarding HMOs, with specific regard to 2’FL and LNnT.

We previously demonstrated in non-human primates (NHP) that Mediterranean diet consumption shifted the proportional abundance of Lactobacillus in the breast and gut. This data highlights a potential link about gut-breast microbiome interconnectivity. To address this question, we compared bacterial populations identified in matched breast and faecal samples from our NHP study. Dietary pattern concurrently shifted two species in both regions; Streptococcus lutetiensis and Ruminococcus torques. While we observe similar trends in Lactobacillus abundances in the breast and gut, the species identified in each region vary; Mediterranean diet increased Lactobacillus_ unspecified species in breast but regulated L. animalis and L. reuteri in the gut. We also investigated the impact of gut permeability on the breast microbiome. Regardless of dietary pattern, subjects that displayed increased physiological measures of gut permeability (elevated plasma lipopolysaccharide, decreased villi length, and decreased goblet cells) displayed a significantly different breast microbiome. Gut barrier dysfunction was associated with increased α-diversity and significant different β-diversity in the breast tissue. Taken together our data supports the presence of a breast microbiome influenced by diet that largely varies from the gut microbiome population but is, however, sensitive to gut permeability.