Összefüggés a bél-hiperpermeabilitás és az elhízás között.

Obesity is a combination of genetic, environmental factors, and systemic inflammation of adipose tissue. In the last decade, more and more evidence suggests that intestinal microbiota is an environmental factor that plays a crucial role in obesity and associated metabolic disorders. Here, we review the association between intestinal microbiota and obesity based on the literature data available to us. The intestinal flora, in the equilibrium state of conventional bacteria, protects the health of the host and helps the development of the immune system. The genome, diet, lifestyle, and epigenetic changes of the host can pathologically alter the composition of the microbiota. In dysbiosis, the development of the gut-associated lymphoid tissue (GALT) associated with the intestinal tract is impaired and the integrity of the intestinal barrier is impaired. Due to the consequent intestinal hyperpermeability, components of pathogenic pathogens such as lipopolysaccharides enter the bloodstream. These components bind to receptors on adipose tissue immune cells as ligands for molecular samples with pathogenic properties and induce adipose tissue dysfunction. The secretion of inflammatory cytokines in adipose tissue is increased. This induces persistent low chronic inflammation, which is responsible for the development of obesity. The damage to health caused by the hyperpermeability of the intestinal barrier can be reduced by interventions, or restored early in the process. Knowing the relationships will help prevent and treat obesity. Orv Hetil. 2022; 163(32): 1261-1267.

RNA Fluorescence in situ Hybridization (FISH) to Visualize Microbial Colonization and Infection in Caenorhabditis elegans Intestines.

The intestines of wild Caenorhabditis nematodes are inhabited by a variety of microorganisms, including gut microbiome bacteria and pathogens, such as microsporidia and viruses. Because of the similarities between Caenorhabditis elegans and mammalian intestinal cells, as well as the power of the C. elegans system, this host has emerged as a model system to study host intestine-microbe interactions in vivo. While it is possible to observe some aspects of these interactions with bright-field microscopy, it is difficult to accurately classify microbes and characterize the extent of colonization or infection without more precise tools. RNA fluorescence in situ hybridization (FISH) can be used as a tool to identify and visualize microbes in nematodes from the wild or to experimentally characterize and quantify infection in nematodes infected with microbes in the lab. FISH probes, labeling the highly abundant small subunit ribosomal RNA, produce a bright signal for bacteria and microsporidian cells. Probes designed to target conserved regions of ribosomal RNA common to many species can detect a broad range of microbes, whereas targeting divergent regions of the ribosomal RNA is useful for narrower detection. Similarly, probes can be designed to label viral RNA. A protocol for RNA FISH staining with either paraformaldehyde (PFA) or acetone fixation is presented. PFA fixation is ideal for nematodes associated with bacteria, microsporidia, and viruses, whereas acetone fixation is necessary for the visualization of microsporida spores. Animals were first washed and fixed in paraformaldehyde or acetone. After fixation, FISH probes were incubated with samples to allow for the hybridization of probes to the desired target. The animals were again washed and then examined on microscope slides or using automated approaches. Overall, this FISH protocol enables detection, identification, and quantification of the microbes that inhabit the C. elegans intestine, including microbes for which there are no genetic tools available.

Using Single-Worm Data to Quantify Heterogeneity in Caenorhabditis elegans-Bacterial Interactions.

The nematode Caenorhabditis elegans is a model system for host-microbe and host-microbiome interactions. Many studies to date use batch digests rather than individual worm samples to quantify bacterial load in this organism. Here it is argued that the large inter-individual variability seen in bacterial colonization of the C. elegans intestine is informative, and that batch digest methods discard information that is important for accurate comparison across conditions. As describing the variation inherent to these samples requires large numbers of individuals, a convenient 96-well plate protocol for disruption and colony plating of individual worms is established.

Human Milk Oligosaccharides Impact Cellular and Inflammatory Gene Expression and Immune Response.

Human milk harbors complex carbohydrates, including human milk oligosaccharides (HMOs), the third most abundant component after lactose and lipids. HMOs have been shown to impact intestinal microbiota, modulate the intestinal immune response, and prevent pathogenic bacterial binding by serving as decoy receptors. However, the direct effect of HMOs on intestinal function and immunity remains to be elucidated. To address this knowledge gap, 21-day-old germ-free mice (C57BI/6) were orally gavaged with 15 mg/day of pooled HMOs for 7 or 14 days and euthanized at day 28 or 35. A set of mice was maintained until day 50 to determine the persistent effects of HMOs. Control groups were maintained in the isolators for 28, 35, or 50 days of age. At the respective endpoints, intestinal tissues were subjected to histomorphometric and transcriptomic analyses, while the spleen and mesenteric lymph nodes (MLNs) were subjected to flow cytometric analysis. The small intestine (SI) crypt was reduced after HMO treatment relative to control at days 28 and 35, while the SI villus height and large intestine (LI) gland depth were decreased in the HMO-treated mice relative to the control at day 35. We report significant HMO-induced and location-specific gene expression changes in host intestinal tissues. HMO treatment significantly upregulated genes involved in extracellular matrix, protein ubiquitination, nuclear transport, and mononuclear cell differentiation. CD4+ T cells were increased in both MLNs and the spleen, while CD8+ T cells were increased in the spleen at day 50 in the HMO group in comparison to controls. In MLNs, plasma cells were increased in HMO group at days 28 and 35, while in the spleen, only at day 28 relative to controls. Macrophages/monocytes and neutrophils were lower in the spleen of the HMO group at days 28, 35, and 50, while in MLNs, only neutrophils were lower at day 50 in the 14-day HMO group. In addition, diphtheria toxoid and tetanus toxoid antibody-secreting cells were higher in HMO-supplemented group compared to controls. Our data suggest that HMOs have a direct effect on gastrointestinal tract metabolism and the immune system even in the absence of host microbiota.

Bacterial community in Sinonovacula constricta intestine and its relationship with culture environment.

Although the importance of intestinal microbes to aquaculture animals has been recognized, the intestinal bacteria of Sinonovacula constricta and its culture environment are rarely studied. In this study, high-throughput sequencing was used to explore the intestinal bacterial communities of pond water, sediment, and S. constricta intestine. Significance analysis and principal coordinates analysis (PCoA) showed that there were significant differences in bacterial communities among animals' intestine, pond water, and sediment (p < 0.05). Venn analysis showed that intestinal bacteria shared a considerable number of OTUs (operational taxonomic units) with the sediment and water. SourceTracker analysis suggested that the contribution of sediment to the intestinal bacteria of S. constricta was much larger than that of rearing water. The Kruskal-Wallis test showed that the dominant bacterial taxa differed significantly between animals' intestines and the pond environment, and each of them has a unique bacterial composition. A network diagram indicated the complex positive and negative interactions between intestinal bacteria at the OTU level. Furthermore, BugBase analysis indicated that the bacterial contribution to potential pathogens in the animals' intestines is similar to that in sediments, suggesting that sediment was the main source of potential pathogens in S. constricta intestine. This study provided a theoretical basis for environmental regulation and disease prevention of S. constricta in aquaculture. KEY POINTS: • Culture environment had a significant effect on the intestinal bacterial community in S. constricta. • Sediment was a major source of intestinal bacteria and potentially pathogenic bacteria. • Complex positive and negative interactions existed between intestinal bacteria.

BATF3 Protects Against Metabolic Syndrome and Maintains Intestinal Epithelial Homeostasis.

The intestinal immune system and microbiota are emerging as important contributors to the development of metabolic syndrome, but the role of intestinal dendritic cells (DCs) in this context is incompletely understood. BATF3 is a transcription factor essential in the development of mucosal conventional DCs type 1 (cDC1). We show that Batf3-/- mice developed metabolic syndrome and have altered localization of tight junction proteins in intestinal epithelial cells leading to increased intestinal permeability. Treatment with the glycolysis inhibitor 2-deoxy-D-glucose reduced intestinal inflammation and restored barrier function in obese Batf3-/- mice. High-fat diet further enhanced the metabolic phenotype and susceptibility to dextran sulfate sodium colitis in Batf3-/- mice. Antibiotic treatment of Batf3-/- mice prevented metabolic syndrome and impaired intestinal barrier function. Batf3-/- mice have altered IgA-coating of fecal bacteria and displayed microbial dysbiosis marked by decreased obesity protective Akkermansia muciniphila, and Bifidobacterium. Thus, BATF3 protects against metabolic syndrome and preserves intestinal epithelial barrier by maintaining beneficial microbiota.

The Role of Probiotics in Alleviating Postweaning Diarrhea in Piglets From the Perspective of Intestinal Barriers.

Early weaning of piglets is an important strategy for improving the production efficiency of sows in modern intensive farming systems. However, due to multiple stressors such as physiological, environmental and social challenges, postweaning syndrome in piglets often occurs during early weaning period, and postweaning diarrhea (PWD) is a serious threat to piglet health, resulting in high mortality. Early weaning disrupts the intestinal barrier function of piglets, disturbs the homeostasis of gut microbiota, and destroys the intestinal chemical, mechanical and immunological barriers, which is one of the main causes of PWD in piglets. The traditional method of preventing PWD is to supplement piglet diet with antibiotics. However, the long-term overuse of antibiotics led to bacterial resistance, and antibiotics residues in animal products, threatening human health while causing dysbiosis of gut microbiota and superinfection of piglets. Antibiotic supplementation in livestock diets is prohibited in many countries and regions. Regarding this context, finding antibiotic alternatives to maintain piglet health at the critical weaning period becomes a real emergency. More and more studies showed that probiotics can prevent and treat PWD by regulating the intestinal barriers in recent years. Here, we review the research status of PWD-preventing and treating probiotics and discuss its potential mechanisms from the perspective of intestinal barriers (the intestinal microbial barrier, the intestinal chemical barrier, the intestinal mechanical barrier and the intestinal immunological barrier) in piglets.

Intestinal changes associated with nitrite exposure in Bufo gargarizans larvae: Histological damage, immune response, and microbiota dysbiosis.

Nitrite is a ubiquitous toxic compound in aquatic ecosystems and has negative effects on aquatic organisms. The intestine and the trillions of microbes that inhabit it, play an integral role in maintaining digestive and immune functions. However, the effects of nitrite on intestinal health and microflora have been poorly investigated. Therefore, the present study evaluated the response of intestinal histology, immunity, digestive enzyme activities and microbiota to nitrite exposure in Bufo gargarizans tadpoles. The results showed that nitrite caused damage to the intestine and impaired digestive performance. Significant changes in the transcriptional profiles of genes involved in oxidative stress (sod, gpx and hsp), inflammation, and immunity (socs3, il-27, il-1ß and il-17d) were observed in the NO2-N treatment groups. In addition, exposure to nitrite induced alterations of intestinal microbial diversity, structure and composition, suggesting that nitrite may lead to intestinal microbiota dysbiosis. It is noteworthy that probiotics (e.g., Bacteroidetes and Fusobacteria) were decreased after exposure to nitrite, whereas potentially opportunistic pathogens such as Proteobacteria and Enterobacteriaceae were elevated. Functional prediction and correlation analysis suggested that the above changes may interfere with metabolic function and trigger various diseases. Taken together, we concluded that nitrite exposure induced intestinal microbial dysbiosis, which may lead to immune dysfunction and metabolic disorder, and ultimately to histological damages in B. gargarizans. Further, this study will provide a scientific basis for further understanding the risk of nitrite pollution on the intestinal health of amphibians.

Intestine-Specific NHE3 Deletion in Adulthood Causes Microbial Dysbiosis.

In the intestine, the Na+/H+ exchanger 3 (NHE3) plays a critical role for Na+ and fluid absorption. NHE3 deficiency predisposes patients to inflammatory bowel disease (IBD). In mice, selective deletion of intestinal NHE3 causes various local and systemic pathologies due to dramatic changes in the intestinal environment, which can influence microbiota colonization. By using metagenome shotgun sequencing, we determined the effect of inducible intestinal epithelial cell-specific deletion of NHE3 (NHE3IEC-KO) in adulthood on the gut microbiome in mice. Compared with control mice, NHE3IEC-KO mice show a significantly different gut microbiome signature, with an unexpected greater diversity. At the phylum level, NHE3IEC-KO mice showed a significant expansion in Proteobacteria and a tendency for lower Firmicutes/Bacteroidetes (F/B) ratio, an indicator of dysbiosis. At the family level, NHE3IEC-KO mice showed significant expansions in Bacteroidaceae, Rikenellaceae, Tannerellaceae, Flavobacteriaceae and Erysipelotrichaceae, but had contractions in Lachnospiraceae, Prevotellaceae and Eubacteriaceae. At the species level, after removing those with lowest occurrence and abundance, we identified 23 species that were significantly expanded (several of which are established pro-inflammatory pathobionts); whereas another 23 species were found to be contracted (some of which are potential anti-inflammatory probiotics) in NHE3IEC-KO mice. These results reveal that intestinal NHE3 deletion creates an intestinal environment favoring the competitive advantage of inflammophilic over anti-inflammatory species, which is commonly featured in conventional NHE3 knockout mice and patients with IBD. In conclusion, our study emphasizes the importance of intestinal NHE3 for gut microbiota homeostasis, and provides a deeper understanding regarding interactions between NHE3, dysbiosis, and IBD.

The intestinal colonization of Lactiplantibacillus plantarum AR113 is influenced by its mucins and intestinal environment.

Lactiplantibacillus plantarum is an important member of the probiotic family and colonization of the host intestinal is essential for its continued probiotic function. The mechanism of L. plantarum intestinal colonization has not been elucidated until now, an important reason being that the colonization process is influenced by a number of factors. In this study, to confirm the influences of adhesion ability and host intestinal environment on L. plantarum intestinal colonization, knockouts of L. plantarum AR113 mucin genes were constructed using CRISPR/Cas9 gene editing technology, and polyethylene glycol was used to reduce the intestinal flora abundance. The knockout of L. plantarum AR113 mucin genes barely altered the strain's tolerance to acid and bile salts. Notably, the adhesion number of AR113ΔLp_1431ΔLp_2233ΔLp_2792 to HT-29 cells was reduced from 175 to 114 per 100 cells. Through in vivo colonization experiments, an increase in the fluorescence intensity of AR113 and AR113ΔLp_1431&2233&2792 was detected the day after the mice were fed, while the deletion of Lp_1431, Lp_2233 and Lp_2792 genes reduced the intestinal tract colonization time from 14 to 11 days. Both AR113 and AR113ΔLp_1431ΔLp_2233ΔLp_2792 were reproduced in the intestine by labeling with 5-(6)-carboxyfluorescein diacetate N-succinimidyl ester. The results showed that the change in fluorescence intensity was closely dependent on the number of adhesions. Finally, compared to the control group, the prolonged intestinal colonization time of AR113ΔLp_1431ΔLp_2233ΔLp_2792 increased mice intestinal flora abundance, with distributions in the duodenum, jejunum, ileum and colon. Collectively, both the intestinal environment and the adhesion ability of L. plantarum AR113 affected intestinal colonization, and the host's intestinal genetic background may be a key factor in the intestinal colonization of L. plantarum.

Gut microbiota alternation under the intestinal epithelium-specific knockout of mouse Piga gene.

Crosstalk between the gut microbiota and intestinal epithelium shapes the gut environment and profoundly influences the intestinal immune homeostasis. Glycosylphosphatidylinositol anchored proteins (GPI - APs) contribute to a variety of gut-associated immune functions, including microbial surveillance and defense, and epithelial cell polarity. Properly polarised epithelial cells are essential for the establishment of the barrier function of gut epithelia. The Piga gene is one among seven genes that encode for an enzyme which is involved in the first step of GPI-anchor biosynthesis. This is the first study reporting a knockout of the intestinal epithelial cell-specific Piga gene (Piga-/-) and its association with the gut microbiota in mice using a whole metagenome shotgun-based sequencing approach. An overall reduced microbiota diversity has been observed in the Piga-/- group as compared to the control group (ANOVA p = 0.34). The taxonomic biomarkers, namely: Gammaproteobacteria (class), Enterobacterales (order), Enterobacteriaceae (family), Escherichia (genus), Proteus (genus) and Escherichia coli (species), increased more in the Piga-/- mice as compared to in the control group. Further, the pathogenic E. coli strains, namely E. coli O157:H7 str. EDL 933 (EHEC), E. coli CFT073 (UPEC) and E. coli 536 (UPEC), were found in the Piga-/- mice which also harbored virulence factor transporters. In addition, the taxa responsible for short chain fatty acid production were decreased in the Piga-/- group. The Piga-/- mice gut harbored an increased number of microbial functions responsible for the survival of pathogens in the inflamed gut environment. Our observations clearly indicate that the Piga-/- mice gut might have an overall enhancement in pathogenic behaviour and reduced capabilities beneficial to health.

The impact of Lactobacillus and Bifidobacterium probiotic cocktail on modulation of gene expression of gap junctions dysregulated by intestinal pathogens.

Probiotics are special bacterial strains with strain specific impacts. They can affect health condition in intestine by producing organic acid, competing with pathogens and maintaining cells homeostasis. Regarding to importance of cell junctions in cells transportation and the influence of pathogens in their functions which lead to inflammation, the impact of probiotic strains comprised of Lactobacillus and Bifidobacterium strains on two important members of gap junctions (Cx26 and Cx43) were assayed. The expressions of cell junction genes in contact with probiotic cocktail along with pathogenic components of enterotoxigenic Escherichia coli and Salmonella typhimurium on HT-29 cell line in different treatment orders were evaluated. Results analysis demonstrated downregulation of cx26 and cx43 along with pathogenic components while, probiotic cocktail could modulate their expression by upregulation. We concluded that Lactobacillus and Bifidobacterium strains were efficient probiotics, when they were used as one cocktail, impacted grater amount on the expression of cell junctions and this might lead to modulate homeostasis and reveal inflammation symptoms in intestine.

Influence of Gluten-Free Diet on Gut Microbiota Composition in Patients with Coeliac Disease: A Systematic Review.

The aim of this study was to assess the changes in microbiota composition during a gluten-free diet (GFD) in coeliac disease (CD) patients. The systematic search followed databases such as PUBMED (MEDLINE), SCOPUS, WEB OF SCIENCE and EMBASE. Out of 843 initially screened papers, a total number of 13 research papers were included. A total of 212 patients with CD on GFD, in comparison to 174 healthy individuals and 176 untreated patients with CD, were examined. Analysis of the microbial community based primarily on faecal samples and duodenal biopsies. Bifidobacterium was noticed to be less abundant in the study group than in both control groups, while the abundance of Bacteroides was more numerous in the group of CD patients on GFD. Staphylococcaceae prevailed in untreated CD patients. Despite the fact that the GFD was not able to fully restore commensal microorganism abundance, the treatment was associated with the greater abundance of selected beneficial bacteria and lower presence of pathogenic bacteria associated with worsening of CD symptoms.

Effects of bowel preparation on intestinal bacterial associated urine and faecal metabolites and the associated faecal microbiome.

BACKGROUND: Urinary and faecal metabolic profiling have been extensively studied in gastrointestinal diseases as potential diagnostic markers, and to enhance our understanding of the intestinal microbiome in the pathogenesis these conditions. The impact of bowel cleansing on the microbiome has been investigated in several studies, but limited to just one study on the faecal metabolome. AIM: To compare the effects of bowel cleansing on the composition of the faecal microbiome, and the urine and faecal metabolome. METHODS: Urine and faecal samples were obtained from eleven patients undergoing colonoscopy at baseline, and then at day 3 and week 6 after colonoscopy. 16S rRNA gene sequencing was used to analyse changes in the microbiome, and metabonomic analysis was performed using proton nuclear magnetic resonance (1H NMR) spectroscopy. RESULTS: Microbiomic analysis demonstrated a reduction in alpha diversity (Shannon index) between samples taken at baseline and three days following bowel cleansing (p = 0.002), and there was no significant difference between samples at baseline and six weeks post colonoscopy. Targeted and non-targeted analysis of urinary and faecal bacterial associated metabolites showed no significant impact following bowel cleansing. CONCLUSIONS: Bowel cleansing causes a temporary disturbance in bacterial alpha diversity measured in faeces, but no significant changes in the faecal and urine metabolic profiles, suggesting that overall the faecal microbiome and its associated metabolome is resistant to the effects of an induced osmotic diarrhoea.

Next-Generation Probiotics for Inflammatory Bowel Disease.

Engineered probiotics represent a cutting-edge therapy in intestinal inflammatory disease (IBD). Genetically modified bacteria have provided a new strategy to release therapeutically operative molecules in the intestine and have grown into promising new therapies for IBD. Current IBD treatments, such as corticosteroids and immunosuppressants, are associated with relevant side effects and a significant proportion of patients are dependent on these therapies, thus exposing them to the risk of relevant long-term side effects. Discovering new and effective therapeutic strategies is a worldwide goal in this research field and engineered probiotics could potentially provide a viable solution. This review aims at describing the proceeding of bacterial engineering and how genetically modified probiotics may represent a promising new biotechnological approach in IBD treatment.

Interspecies commensal interactions have nonlinear impacts on host immunity.

The impacts of individual commensal microbes on immunity and disease can differ dramatically depending on the surrounding microbial context; however, the specific bacterial combinations that dictate divergent immunological outcomes remain largely undefined. Here, we characterize an immunostimulatory Allobaculum species from an inflammatory bowel disease patient that exacerbates colitis in gnotobiotic mice. Allobaculum inversely associates with the taxonomically divergent immunostimulatory species Akkermansia muciniphila in human-microbiota-associated mice and human cohorts. Co-colonization with A. muciniphila ameliorates Allobaculum-induced intestinal epithelial cell activation and colitis in mice, whereas Allobaculum blunts the A.muciniphila-specific systemic antibody response and reprograms the immunological milieu in mesenteric lymph nodes by blocking A.muciniphila-induced dendritic cell activation and T cell expansion. These studies thus identify a pairwise reciprocal interaction between human gut bacteria that dictates divergent immunological outcomes. Furthermore, they establish a generalizable framework to define the contextual cues contributing to the "incomplete penetrance" of microbial impacts on human disease.

A multistrain probiotic improves handgrip strength and functional capacity in patients with COPD: A randomized controlled trial.

PURPOSE: The age-related muscle loss, termed sarcopenia and functional dependency, are common findings in patients with chronic obstructive pulmonary disease (COPD). However, an effective bedside treatment remains elusive. OBJECTIVE: To assess the effects of probiotics on sarcopenia and physical capacity in COPD patients. METHODS: Randomized, double-blind, computer-controlled, multicenter trial in two tertiary-care hospitals for 16 weeks. A central computer system randomly allocated male, 63-73 years old COPD patients into placebo (n=53) and probiotic (n=51) groups. The intervention was Vivomix 112 billion*, one capsule a day for 16 weeks. The main outcomes measured were sarcopenia phenotype, short physical performance battery (SPPB), plasma markers of intestinal permeability (zonulin and claudin-3) and neuromuscular junction degradation (CAF22), body composition, and handgrip strength (HGS) before and following the probiotics treatment. FINDINGS: 4 patients discontinued intervention due to poor compliance and 100 patients, including placebo (n=53) and probiotic (n=47) groups were analyzed. Probiotics reduced plasma zonulin, claudin-3, and CAF22, along with an improvement in HGS, gait speed, and SPPB scores (all p<0.05). Probiotic treatment also reduced the plasma c-reactive proteins and 8-isoprostane levels, the markers of systemic inflammation and oxidative stress (p<0.05). Correlation analysis revealed varying degrees of association of plasma biomarkers with sarcopenia indexes. Despite a statistical trend, we did not find a reduction in sarcopenia prevalence in the probiotic group. CONCLUSION: Taken together, the multistrain probiotic improves muscle strength and functional performance in COPD patients by reducing intestinal permeability and stabilizing neuromuscular junction. TRIAL REGISTRATION: GMC clinical trial unit, GMC-CREC-00263.

Glucosylceramide Changes Bacterial Metabolism and Increases Gram-Positive Bacteria through Tolerance to Secondary Bile Acids In Vitro.

Glucosylceramide is present in many foods, such as crops and fermented foods. Most glucosylceramides are not degraded or absorbed in the small intestine and pass through the large intestine. Glucosylceramide exerts versatile effects on colon tumorigenesis, skin moisture, cholesterol metabolism and improvement of intestinal microbes in vivo. However, the mechanism of action has not yet been fully elucidated. To gain insight into the effect of glucosylceramide on intestinal microbes, glucosylceramide was anaerobically incubated with the dominant intestinal microbe, Blautia coccoides, and model intestinal microbes. The metabolites of the cultured broth supplemented with glucosylceramide were significantly different from those of broth not treated with glucosylceramide. The number of Gram-positive bacteria was significantly increased upon the addition of glucosylceramide compared to that in the control. Glucosylceramide endows intestinal microbes with tolerance to secondary bile acid. These results first demonstrated that glucosylceramide plays a role in the modification of intestinal microbes.

A newly isolated human intestinal strain deglycosylating flavonoid C-glycosides.

Glycosidic bond of C-glycosides is difficult to be broken due to its chemical stability. Screening specific microbe from microbiota is a practical way to deglycosylate these compounds. In this study, a new strain W974-1 which is capable of cleaving C-glycosidic bonds was isolated from human gut microbiota by spread plate method. It deglycosylates flavonoid 8-C-glycosides such as orientin and vitexin to their aglycones with the enzymes secreted outside the bacterial cells. This strain was identified as Enterococcus avium by 16S rDNA sequencing, physiological and biochemical characterization.

Current Advances in Structure-Function Relationships and Dose-Dependent Effects of Human Milk Oligosaccharides.

HMOs (human milk oligosaccharides) are the third most important nutrient in breast milk. As complex glycans, HMOs play an important role in regulating neonatal intestinal immunity, resisting viral and bacterial infections, displaying anti-inflammatory characteristics, and promoting brain development. Although there have been some previous reports of HMOs, a detailed literature review summarizing the structure-activity relationships and dose-dependent effects of HMOs is lacking. Hence, after introducing the structures and synthetic pathways of HMOs, this review summarizes and categorizes identified structure-function relationships of HMOs. Differential mechanisms of different structural HMOs utilization by microorganisms are summarized. This review also emphasizes the recent advances in the interactions between different health benefits and the variance of dosage effect based on in vitro cell tests, animal experiments, and human intervention studies. The potential relationships between the chemical structure, the dosage selection, and the physiological properties of HMOs as functional foods are vital for further understanding of HMOs and their future applications.