Probiotics, Prebiotics, and Synbiotics in the Irritable Bowel Syndrome Treatment: A Review.

Irritable bowel syndrome is not a life-threatening disease, yet it significantly affects the quality of life and contributes to economic loss. It is estimated that even up to 45% of the world's population can suffer from the disease. The first attempts to diagnose irritable bowel syndrome were made at the end of the 19th century; however, establishing appropriate diagnostic criteria and treatment methods is still ongoing. To date, little is known about the etiology of irritable bowel syndrome; however, growing attention is drawn to the intestinal microbiota as a factor in the disease development. For this reason, researchers have conducted many studies on therapies that modulate the microbiota, among which probiotics, prebiotics, and synbiotics are widely studied. To date, most studies have examined probiotics; however, there are also several studies demonstrating the efficacy of prebiotics and synbiotics. The aim of this review was to summarize findings on the usefulness of probiotics, prebiotics, and synbiotics in the treatment of irritable bowel syndrome.

One dog's waste is another dog's wealth: A pilot study of fecal microbiota transplantation in dogs with acute hemorrhagic diarrhea syndrome.

Canine acute hemorrhagic diarrhea syndrome (AHDS) has been associated in some studies with Clostridioides perfringens overgrowth and toxin-mediated necrosis of the intestinal mucosa. We aimed to determine the effect of a single fecal microbiota transplantation (FMT) on clinical scores and fecal microbiomes of 1 and 7 dogs with AHDS from New Zealand and South Africa. We hypothesized that FMT would improve AHDS clinical scores and increase microbiota alpha-diversity and short-chain fatty acid (SCFA)-producing microbial communities' abundances in dogs with AHDS after FMT. We sequenced the V3-V4 region of the 16S-rRNA gene in the feces of AHDS FMT-recipients and sham-treated control dogs, and their healthy donors at admission, discharge, and 30 days post-discharge. There were no significant differences in median AHDS clinical scores between FMT-recipients and sham-treated controls at admission or discharge (P = 0.22, P = 0.41). At admission, the Shannon diversity index (SDI) was lower in AHDS dogs than healthy donors (P = 0.002). The SDI did not change from admission to 30 days in sham-treated dogs yet increased in FMT-recipients from admission to discharge (P = 0.04) to levels not different than donors (P = 0.33) but significantly higher than sham-treated controls (P = 0.002). At 30 days, the SDI did not differ between FMT recipients, sham-treated controls, and donors (P = 0.88). Principal coordinate analysis of the Bray-Curtis index separated post-FMT and donor dogs from pre-FMT and sham-treated dogs (P = 0.009) because of increased SCFA-producing genera's abundances after FMT. A single co-abundance subnetwork contained many of the same OTUs found to be differentially abundant in FMT-recipients, and the abundance of this module was increased in FMT-recipients at discharge and 30 days, compared to sham-treated controls. We conclude in this small pilot study FMT did not have any clinical benefit. A single FMT procedure has the potential to increase bacterial communities of SCFA-producing genera important for intestinal health up to 30 days post-FMT.

Dried yeast cell walls high in beta-glucan and mannan-oligosaccharides positively affect microbial composition and activity in the canine gastrointestinal tract in vitro.

The outer cell wall of yeast is characterized by high levels of ß-glucans and mannan-oligosaccharides (MOS), which have been linked with beneficial effects on intestinal health and immune status in dogs. In this study, a standardized in vitro simulation of the canine gastrointestinal tract (Simulator of the Canine Intestinal Microbial Ecosystem; SCIME) was used to evaluate the effect of a Saccharomyces cerevisiae-based product, consisting of 27.5% ß-glucans and 22.5% MOS, on the activity (as assessed by measurement of fermentative metabolites) and composition (as assessed by 16S-targeted Illumina sequencing) of canine intestinal microbiota. The S. cerevisiae-based product was tested at three different dosages, i.e., 0.5, 1.0, and 2.0 g/d. A dose-dependent fermentation pattern was observed along the entire length of the colon, as shown by the increased production of the health-related acetate, propionate, and butyrate for the three concentrations tested (0.5, 1.0, and 2.0 g/d). A consistent finding for all three tested concentrations was the increased propionate production (P < 0.05) in the simulated proximal and distal colon. These changes in terms of fermentative metabolites could be linked to specific microbial alterations at the family level, such as the specific stimulation of the propionate-producing families Porphyromonadaceae and Prevotellaceae upon in vitro exposure to the S. cerevisiae-based product. Other consistent changes in community composition upon repeated exposure included the decrease in the Enterobacteriaceae and the Fusobacteriaceae families, which both contain several potentially opportunistic pathogens. Altogether, the generated data support a possible health-promoting role of a product high in ß-glucans and MOS when supplemented to the dogs' diet.

Diarrhoeal events can trigger long-term Clostridium difficile colonization with recurrent blooms.

Although Clostridium difficile is widely considered an antibiotic- and hospital-associated pathogen, recent evidence indicates that this is an insufficient depiction of the risks and reservoirs. A common thread that links all major risk factors of infection is their association with gastrointestinal disturbances, but this relationship to C. difficile colonization has never been tested directly. Here, we show that disturbances caused by diarrhoeal events trigger susceptibility to C. difficile colonization. Using survey data of the human gut microbiome, we detected C. difficile colonization and blooms in people recovering from food poisoning and Vibrio cholerae infections. Carriers remained colonized for year-long time scales and experienced highly variable patterns of C. difficile abundance, where increased shedding over short periods of 1-2 d interrupted week-long periods in which C. difficile was undetectable. Given that short shedding events were often linked to gastrointestinal disturbances, our results help explain why C. difficile is frequently detected as a co-infecting pathogen in patients with diarrhoea. To directly test the impact of diarrhoea on susceptibility to colonization, we developed a mouse model of variable disturbance intensity, which allowed us to monitor colonization in the absence of disease. As mice exposed to avirulent C. difficile spores ingested increasing quantities of laxatives, more individuals experienced C. difficile blooms. Our results indicate that the likelihood of colonization is highest in the days immediately following acute disturbances, suggesting that this could be an important window during which transmission could be interrupted and the incidence of infection lowered.

Impact of Enterobius vermicularis infection and mebendazole treatment on intestinal microbiota and host immune response.

BACKGROUND: Previous studies on the association of enterobiasis and chronic inflammatory diseases have revealed contradictory results. The interaction of Enterobius vermicularis infection in particular with gut microbiota and induced immune responses has never been thoroughly examined. METHODOLOGY/FINDINGS: In order to answer the question of whether exposure to pinworm and mebendazole can shift the intestinal microbial composition and immune responses, we recruited 109 (30 pinworm-negative, 79 pinworm-infected) first and fourth grade primary school children in Taichung, Taiwan, for a gut microbiome study and an intestinal cytokine and SIgA analysis. In the pinworm-infected individuals, fecal samples were collected again at 2 weeks after administration of 100 mg mebendazole. Gut microbiota diversity increased after Enterobius infection, and it peaked after administration of mebendazole. At the phylum level, pinworm infection and mebendazole deworming were associated with a decreased relative abundance of Fusobacteria and an increased proportion of Actinobacteria. At the genus level, the relative abundance of the probiotic Bifidobacterium increased after enterobiasis and mebendazole treatment. The intestinal SIgA level was found to be lower in the pinworm-infected group, and was elevated in half of the mebendazole-treated group. A higher proportion of pre-treatment Salmonella spp. was associated with a non-increase in SIgA after mebendazole deworming treatment. CONCLUSIONS/SIGNIFICANCE: Childhood exposure to pinworm plus mebendazole is associated with increased bacterial diversity, an increased abundance of Actinobacteria including the probiotic Bifidobacterium, and a decreased proportion of Fusobacteria. The gut SIgA level was lower in the pinworm-infected group, and was increased in half of the individuals after mebendazole deworming treatment.

Contributions of the Interaction Between Dietary Protein and Gut Microbiota to Intestinal Health.

There is growing recognition that composition and metabolic activity of the gut microbiota can be modulated by the dietary proteins which in turn impact health. The amino acid composition and digestibility of proteins, which are influenced by its source and amount of intake, play a pivotal role in determining the microbiota. Reciprocally, it appears that the gut microbiota is also able to affect protein metabolism which gives rise to the view that function between the microbiota and protein can proceed in both directions. In response to the alterations in dietary protein components, there are significant changes in the microbial metabolites including short chain fatty acids (SCFAs), ammonia, amines, gases such as hydrogen, sulfide and methane which are cytotoxins, genotoxins and carcinogens associated with development of colon cancer and inflammatory bowel diseases. A suitable ratio between protein and carbohydrate or even a low protein diet is recommended based on the evidence that excessive protein intake adversely affects health. Supplying high and undigested proteins will encourage pathogens and protein-fermenting bacteria to increase the risk of diseases. These changes of microbiota can affect the gut barrier and the immune system by regulating gene expression in relevant signaling pathways and by regulating the secretion of metabolites. The objective of this review is to assess the impact of dietary proteins on microbiota composition and activity in the gastrointestinal tract. Attention should be given to the dietary strategies with judicious selection of source and supplementation of dietary protein to benefit gut health.