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Aging Jun 2024Acute pancreatitis (AP) is a prevalent acute abdominal condition, and AP induced colonic barrier dysfunction is commonly observed. Total flavonoids of (TFC) have...
BACKGROUND
Acute pancreatitis (AP) is a prevalent acute abdominal condition, and AP induced colonic barrier dysfunction is commonly observed. Total flavonoids of (TFC) have exhibited noteworthy anti-inflammatory and anti-apoptotic properties.
METHODS
We established AP models, both in animals and cell cultures, employing Cerulein. 16S rRNA gene sequencing was performed to investigate the gut microorganisms changes.
RESULTS
, TFC demonstrated a remarkable capacity to ameliorate AP, as indicated by the inhibition of serum amylase, myeloperoxidase (MPO) levels, and the reduction in pancreatic tissue water content. Furthermore, TFC effectively curtailed the heightened inflammatory response. The dysfunction of colonic barrier induced by AP was suppressed by TFC. At the level, TFC treatment resulted in attenuation of increased cell apoptosis, and regulation of apoptosis related proteins expression in AR42J cells. The increase of , , , and by AP, and decrease of of , , by AP were both reversed by TFC treatment.
CONCLUSIONS
TFC can effectively suppress AP progression and AP induced colonic barrier dysfunction by mitigating elevated serum amylase, MPO levels, water content in pancreatic tissue, as well as curtailing inflammation, apoptosis. The findings presented herein shed light on the potential mechanisms by which TFC inhibit the development of AP progression and AP induced colonic barrier dysfunction.
Topics: Animals; Gastrointestinal Microbiome; Chrysanthemum; Pancreatitis; Flavonoids; Male; Rats; Colon; Apoptosis; Disease Models, Animal; Cell Line; Intestinal Mucosa
PubMed: 38862253
DOI: 10.18632/aging.205924 -
Carbohydrate Polymers Sep 2024Epimedium, a traditional Chinese medicine commonly used as a dietary supplement, contains polysaccharides and flavonoids as its main bioactive ingredients. In this...
Epimedium, a traditional Chinese medicine commonly used as a dietary supplement, contains polysaccharides and flavonoids as its main bioactive ingredients. In this study, a neutral homogeneous polysaccharide (EPSN-1) was isolated from Epimedium brevicornu Maxim. EPSN-1 was identified as a glucan with a backbone of →4)-α-D-Glcp-(1→, branched units comprised α-D-Glcp-(1→6)-α-D-Glcp-(1→, β-D-Glcp-(1→6)-β-D-Glcp-(1→ and α-D-Glcp-(1→ connected to the C6 position of backbone. The conformation of EPSN-1 in aqueous solution indicated its potential to form nanoparticles. This paper aims to investigate the carrier and pharmacodynamic activity of EPSN-1. The findings demonstrated that, on the one hand, EPSN-1, as a functional ingredient, may load Icariin (ICA) through non-covalent interactions, improving its biopharmaceutical properties such as solubility and stability, thereby improving its intestinal absorption. Additionally, as an effective ingredient, EPSN-1 could help maintain the balance of the intestinal environment by increasing the abundance of Parabacteroides, Lachnospiraceae UGG-001, Anaeroplasma, and Eubacterium xylanophilum group, while decreasing the abundance of Allobaculum, Blautia, and Adlercreutzia. Overall, this dual action of EPSN-1 sheds light on the potential applications of natural polysaccharides, highlighting their dual role as carriers and contributors to biological activity.
Topics: Epimedium; Male; Glucans; Prostatic Hyperplasia; Flavonoids; Animals; Drug Carriers; Humans; Gastrointestinal Microbiome
PubMed: 38858029
DOI: 10.1016/j.carbpol.2024.122316 -
International Journal of Biological... Jun 2024Trehalose (α-d-glucopyranosyl-(1-1)-α-D-glucopyranoside) has found applications in diverse food products as a sweetener, stabilizer, and humectant. Recent attention...
Trehalose (α-d-glucopyranosyl-(1-1)-α-D-glucopyranoside) has found applications in diverse food products as a sweetener, stabilizer, and humectant. Recent attention has focused on trehalose due to its contradictory effects on the virulence of Clostridium difficile. In this study, we investigate the impact of novel trehalose-derived galactooligosaccharides (Treh-GOS) on the human gut microbiota using in vitro fecal fermentation models. Distinct Treh-GOS structures elicit varying taxonomic responses. For instance, β-Gal-(1-4)-trehalose [DP3(1-4)] leads to an increase of Bifidobacterium, comparable to results observed with commercial GOS. Conversely, β-Gal-(1-6)-trehalose [DP3(1-6)] prompts an increase in Lactobacillus. Notably, both of these trisaccharides yield the highest concentrations of butyric acid across all samples. On the other hand, Treh-GOS tetrasaccharide mixture (DP4), featuring a novel trehalose galactosylation in both glucose units, fosters the growth of Parabacteroides. Our findings underscore the capacity of novel Treh-GOS to modulate the human gut microbiota. Consequently, these innovative galactooligosaccharides emerge as promising candidates for novel prebiotic applications.
PubMed: 38857723
DOI: 10.1016/j.ijbiomac.2024.133053 -
Frontiers in Microbiology 2024The aim of the study is to investigate the function and mechanism of Zinc Gluconate (ZG) on intestinal mucosal barrier damage in antibiotics and Lipopolysaccharide...
OBJECTIVE
The aim of the study is to investigate the function and mechanism of Zinc Gluconate (ZG) on intestinal mucosal barrier damage in antibiotics and Lipopolysaccharide (LPS)-induced mice.
METHODS
We established a composite mouse model by inducing intestinal mucosal barrier damage using antibiotics and LPS. The animals were divided into five groups: Control (normal and model) and experimental (low, medium, and high-dose ZG treatments). We evaluated the intestinal mucosal barrier using various methods, including monitoring body weight and fecal changes, assessing pathological damage and ultrastructure of the mouse ileum, analyzing expression levels of tight junction (TJ)-related proteins and genes, confirming the TLR4/NF-κB signaling pathway, and examining the structure of the intestinal flora.
RESULTS
In mice, the dual induction of antibiotics and LPS led to weight loss, fecal abnormalities, disruption of ileocecal mucosal structure, increased intestinal barrier permeability, and disorganization of the microbiota structure. ZG restored body weight, alleviated diarrheal symptoms and pathological damage, and maintained the structural integrity of intestinal epithelial cells (IECs). Additionally, ZG reduced intestinal mucosal permeability by upregulating TJ-associated proteins (ZO-1, Occludin, Claudin-1, and JAM-A) and downregulating MLCK, thereby repairing intestinal mucosal barrier damage induced by dual induction of antibiotics and LPS. Moreover, ZG suppressed the TLR4/NF-κB signaling pathway, demonstrating anti-inflammatory properties and preserving barrier integrity. Furthermore, ZG restored gut microbiota diversity and richness, evidenced by increased Shannon and Observed features indices, and decreased Simpson's index. ZG also modulated the relative abundance of beneficial human gut bacteria (, , , , , and ) and harmful bacteria ( and ), repairing the damage induced by dual administration of antibiotics and LPS.
CONCLUSION
ZG attenuates the dual induction of antibiotics and LPS-induced intestinal barrier damage and also protects the intestinal barrier function in mice.
PubMed: 38855764
DOI: 10.3389/fmicb.2024.1407091 -
Frontiers in Pharmacology 2024The prevalence of major depressive disorder (MDD) has gradually increased and has attracted widespread attention. The aim of this study was to investigate the effect of...
coagulans and butyricum synergistically alleviate depression in a chronic unpredictable mild stress mouse model through altering gut microbiota and prefrontal cortex gene expression.
The prevalence of major depressive disorder (MDD) has gradually increased and has attracted widespread attention. The aim of this study was to investigate the effect of a probiotic compound consisting of and , on a mouse depression model. Mice were subjected to chronic unpredictable mild stress (CUMS) and then treated with the probiotics at different concentrations. And mice received behavior test such as forced swimming test and tail suspension test. After that, all mice were sacrificed and the samples were collected for analysis. Moreover, prefrontal cortex (PFC) gene expression and the gut microbiota among different groups were also analyzed. Probiotics improved depressive-like behavior in CUMS mice, as indicated by decreased immobility time ( < 0.05) in the forced swimming test and tail suspension test. probiotics intervention also increased the level of 5-hydroxytryptamine (5-HT) in the prefrontal cortex and decreased the adrenocorticotropic hormone (ACTH) level in serum. In addition, by comparing the PFC gene expression among different groups, we found that the genes upregulated by probiotics were enriched in the PI3K-Akt signaling pathway in the prefrontal cortex. Moreover, we found that downregulated genes in prefrontal cortex of CUMS group such as and , which were correlated with depression, were reversed by the probiotics. Furthermore, the probiotics altered the structure of the gut microbiota, and reversed the reduction of cob(II)yrinate a,c-diamide biosynthesis I pathway in CUMS group. Several species like Bacteroides caecimuris and Parabacteroides distasoni, whose abundance was significantly decreased in the CUMS group but reversed after the probiotics intervention, showed significantly positive correlation with depression associated genes such as and . These findings suggested that CUMS-induced depression-like behavior can be alleviated by the probiotics, possibly through alterations in the PFC gene expression and gut microbiota.
PubMed: 38855745
DOI: 10.3389/fphar.2024.1393874 -
BMC Microbiology Jun 2024Bacteroides fragilis group (BFG) species are the most significant anaerobic pathogens and are also the most antibiotic-resistant anaerobic species. Therefore, surveying...
Detection of the antibiotic resistance genes content of intestinal Bacteroides, Parabacteroides and Phocaeicola isolates from healthy and carbapenem-treated patients from European countries.
BACKGROUND
Bacteroides fragilis group (BFG) species are the most significant anaerobic pathogens and are also the most antibiotic-resistant anaerobic species. Therefore, surveying their antimicrobial resistance levels and investigating their antibiotic resistance mechanisms is recommended. Since their infections are endogenous and they are important constituents of the intestinal microbiota, the properties of the intestinal strains are also important to follow. The aim of this study was to investigate the main antibiotic gene content of microbiota isolates from healthy people and compare them with the gene carriage of strains isolated from infections.
RESULTS
We detected 13, mainly antibiotic resistance determinants of 184 intestinal BFG strains that were isolated in 5 European countries (Belgium, Germany, Hungary, Slovenia and Turkey) and compared these with values obtained earlier for European clinical strains. Differences were found between the values of this study and an earlier one for antibiotic resistance genes that are considered to be mobile, with higher degrees for cfxA, erm(F) and tet(Q) and with lower degrees for msrSA, erm(B) and erm(G). In addition, a different gene prevalence was found depending on the taxonomical groups, e.g., B. fragilis and NBFB. Some strains with both the cepA and cfiA β-lactamase genes were also detected, which is thought to be exceptional since until now, the B. fragilis genetic divisions were defined by the mutual exclusion of these two genes.
CONCLUSIONS
Our study detected the prevalences of a series of antibiotic resistance genes in intestinal Bacteroides strains which is a novelty. In addition, based on the current and some previous data we hypothesized that prevalence of some antibiotic resistance genes detected in the clinical and intestinal BFG strains were different, which could be accounted with the differential composition of the Bacteroides microbiota and/or the MGE mobilities at the luminal vs. mucosal sites of the intestine.
Topics: Humans; Europe; Anti-Bacterial Agents; Carbapenems; Bacteroides Infections; Bacteroides; Drug Resistance, Bacterial; Gastrointestinal Microbiome; Microbial Sensitivity Tests; Genes, Bacterial; Intestines; Bacterial Proteins
PubMed: 38851699
DOI: 10.1186/s12866-024-03354-w -
Molecular Neurobiology Jun 2024Dysbiosis of the gut microbiota is closely associated with neurodegenerative diseases, including Huntington's disease (HD). Gut microbiome-derived metabolites are key...
Dysbiosis of the gut microbiota is closely associated with neurodegenerative diseases, including Huntington's disease (HD). Gut microbiome-derived metabolites are key factors in host-microbiome interactions. This study aimed to investigate the crucial gut microbiome and metabolites in HD and their correlations. Fecal and serum samples from 11 to 26 patients with HD, respectively, and 16 and 23 healthy controls, respectively, were collected. The fecal samples were used for shotgun metagenomics while the serum samples for metabolomics analysis. Integrated analysis of the metagenomics and metabolomics data was also conducted. Firmicutes, Bacteroidota, Proteobacteria, Uroviricota, Actinobacteria, and Verrucomicrobia were the dominant phyla. At the genus level, the presence of Bacteroides, Faecalibacterium, Parabacteroides, Alistipes, Dialister, and Christensenella was higher in HD patients, while the abundance of Lachnospira, Roseburia, Clostridium, Ruminococcus, Blautia, Butyricicoccus, Agathobaculum, Phocaeicola, Coprococcus, and Fusicatenibacter decreased. A total of 244 differential metabolites were identified and found to be enriched in the glycerophospholipid, nucleotide, biotin, galactose, and alpha-linolenic acid metabolic pathways. The AUC value from the integrated analysis (1) was higher than that from the analysis of the gut microbiota (0.8632). No significant differences were found in the ACE, Simpson, Shannon, Sobs, and Chao indexes between HD patients and controls. Our study determined crucial functional gut microbiota and potential biomarkers associated with HD pathogenesis, providing new insights into the role of the gut microbiota-brain axis in HD occurrence and development.
PubMed: 38850348
DOI: 10.1007/s12035-024-04271-9 -
Combinatorial Chemistry & High... Jun 2024In lung adenocarcinoma (LUAD), Qi-deficiency and Phlegm-turbid stagnation (QP) are the most prevalent Traditional Chinese medicine (TCM) syndrome.
BACKGROUND
In lung adenocarcinoma (LUAD), Qi-deficiency and Phlegm-turbid stagnation (QP) are the most prevalent Traditional Chinese medicine (TCM) syndrome.
METHODS
Herein, we collected 90 fecal samples (Healthy individual (H): 30; other syndrome (O): 30; QP: 30) and explored the composition and diversity of gut microbiota in LUAD patients with QP syndrome using 16s-rRNA sequencing. Then, we identified biomarkers for QP syndrome in LUAD patients with linear discriminant analysis (LDA) effect size (LEfSe) and applied logistic regression analysis to construct a diagnostic model evaluated with the area under the receiver operating characteristic curve (AUC) and validated with data from metagenomics.
RESULTS
The α diversity and β diversity revealed that the microbiota community structure in LUAD patients with QP syndrome was different from that with healthy individuals and LUAD patients with other syndromes. At the phylum level, the QP group had more abundance of Bacteroidetes and less Proteobacteria than the O group. At the genus level, the abundance of 4 genera (Bacteroides, Parabacteroides, Prevotella, and Flavonifractor) was different between the QP group and O group. Moreover, LEfSe indicated that those 4 genera might be the biomarkers for LUAD patients with QP syndrome. Then, we used those 4 genera to develop a diagnostic model. The AUC based on 16s-rRNA sequencing and metagenomics was 0.989 and 1, respectively.
CONCLUSION
A diagnostic model was developed, which would be an available tool for the clinical diagnosis of LUAD with QP syndrome.
PubMed: 38847243
DOI: 10.2174/0113862073303081240521083505 -
Gut Microbes 2024Comensal () and are often linked to gut inflammation. However, the causes for variability of pro-inflammatory surface antigens that affect gut commensal/opportunistic...
Comensal () and are often linked to gut inflammation. However, the causes for variability of pro-inflammatory surface antigens that affect gut commensal/opportunistic dualism in remain unclear. By using the classical lipopolysaccharide/O-antigen ' operon' in as a surface antigen model (5-gene-cluster ), and a recent typing strategy for strain classification, we characterized the integrity and conservancy of the entire operon in . Through exploratory analysis of complete genomes and metagenomes, we discovered that most have the operon fragmented into nonrandom patterns of gene-singlets and doublets/triplets, termed 'gene-clusters', or rfb-'minioperons' if predicted as transcriptional. To reflect global operon integrity, contiguity, duplication, and fragmentation principles, we propose a six-category (infra/supra-numerary) cataloging system and a Global Operon Profiling System for bacteria. Mechanistically, genomic sequence analyses revealed that operon fragmentation is driven by intra-operon insertions of predominantly -DNA () and likely natural selection in gut-wall specific micro-niches or micropathologies. -insertions, also detected in other antigenic operons (fimbriae), but not in operons deemed essential (ribosomal), could explain why have fewer KEGG-pathways despite large genomes. DNA insertions, overrepresenting DNA-exchange-avid () species, impact our interpretation of functional metagenomics data by inflating by inflating gene-based pathway inference and by overestimating 'extra-species' abundance. Of disease relevance, species isolated from cavitating/cavernous fistulous tract (CavFT) microlesions in Crohn's Disease have supra-numerary fragmented operons, stimulate TNF-alpha from macrophages with low potency, and do not induce hyperacute peritonitis in mice compared to CavFT . The impact of 'foreign-DNA' insertions on pro-inflammatory operons, metagenomics, and commensalism/opportunism requires further studies to elucidate their potential for novel diagnostics and therapeutics, and to elucidate the role of co-existing pathobionts in Crohn's disease microlesions.
Topics: Operon; Mice; Gastrointestinal Microbiome; Animals; Humans; Metagenomics; Crohn Disease; Bacteroidetes; Antigens, Bacterial; Genome, Bacterial; Enterobacteriaceae
PubMed: 38841888
DOI: 10.1080/19490976.2024.2350150 -
Frontiers in Nutrition 2024The intricate interplay between dietary habits and the development of Parkinson's Disease (PD) has long been a subject of scientific inquiry. Mendelian Randomization...
BACKGROUND
The intricate interplay between dietary habits and the development of Parkinson's Disease (PD) has long been a subject of scientific inquiry. Mendelian Randomization (MR) emerges as a potent tool, harnessing genetic variants to infer causality in observational data. While evidence links diet to Parkinson's Disease (PD) etiology, a thorough MR exploration of dietary impacts on PD, particularly involving gut microbiota, is still emerging.
METHODS
This research leverages the IEU Open GWAS project's vast GWAS database to address the knowledge gap in understanding diet's influence on PD, employing a diverse range of dietary variables. Our holistic dataset includes various foods like processed fava beans, bap, red wine, to cheese, reflecting a commitment to untangling dietary complexities in PD etiology. Advancing from initial dietary-PD associations, we innovatively explore the gut microbiota, focusing on in relation to bap intake and PD, employing MR. Utilizing weighted median, MR-Egger, and inverse variance weighting methods, we ensure rigorous causality assessments, meticulously mitigating pleiotropy and heterogeneity biases to uphold finding validity.
RESULTS
Our findings indicate red wine (OR: 1.031; 95% CI 1.001-1.062; = 0.044) and dried fruit consumption (OR: 2.019; 95% CI 1.052-3.875; = 0.035) correlate with increased PD risk, whereas broad beans (OR: 0.967; 95% CI 0.939-0.996; = 0.024) and bap intake (OR: 0.922; 95% CI 0.860-0.989; = 0.023) show protective effects against PD. Employing MR, specifically the IVW method, revealed a significant inverse association between bap intake and gut microbiota, marked by an 8.010-fold decrease in per standard deviation increase in bap intake (95% CI 1.005-63.818, = 0.049). Furthermore, a connection between PD and was observed (OR: 0.810; 95% CI 0.768-0.999; = 0.049), suggesting a potential microbiota-mediated pathway in PD etiology.
CONCLUSION
Our study links dietary habits to PD risk, showing higher PD risk with red wine and dried fruit consumption, and a protective effect from broad beans and bap. Using MR, we found bap intake inversely correlates with in the gut, suggesting bap influences microbiota. Further, higher levels correlate with lower PD risk, highlighting a complex interplay of diet, gut microbiome, and neurological health. These insights shed light on potential dietary interventions for PD.
PubMed: 38840699
DOI: 10.3389/fnut.2024.1273874