Richness Of Gut Microbiota Research Articles

The gut microbiome and metabolites are altered and interrelated in patients with functional constipation.

Gut microbiota and metabolites have been identified to contribute to the pathogenesis of functional constipation (FC); however, the underlying mechanism(s) have not been elucidated, and the relationship between the gut microbiota and metabolites in FC has received limited attention in the literature. 16S rDNA sequencing and non-targeted metabolomic detection based on liquid chromatography-mass spectrometry (LC-MS/MS) technologies were combined to analyze the altered gut microbiome and metabolic profile of fecal samples from FC patients and healthy individuals (healthy control; HC). The richness and diversity of gut microbiota significantly (p < 0.01) increased in FC patients. Compared to the HC group, 18 genera, including Intestinibacter, Klebsiella, and Akkermansia, exhibited statistically significant changes (p < 0.05). Metabolic analysis showed that metabolic profiles were also markedly altered with 79 metabolites, such as (-)-caryophyllene oxide, chenodeoxycholic acid, and biliverdin, indicating significant inter-group differences (p < 0.05). Besides, the primary bile acid biosynthesis, as well as the metabolic profile of porphyrin and chlorophyll, were the most dominant enriched pathways (FDR < 0.01), in which chenodeoxycholic acid and biliverdin were significantly enriched, respectively. Correlation analysis demonstrated a strong relationship between 10 genera and 19 metabolites (r > 0.6, FDR < 0.05), and notably, Intestinibacter showed a negative correlation with biliverdin (FDR < 0.001), which highlighted the interplay of the gut microbiota and metabolites in the pathogenesis of FC. Our research describes the characteristics of the gut microbiota and metabolic profiles and the correlation between the gut microbiota and metabolites in FC patients. This may contribute to the understanding of the underlying mechanisms involved in FC pathogenesis and may provide novel insights into therapeutic interventions.

Selenium attenuated food borne cadmium-induced intestinal inflammation in red swamp crayfish (Procambarus clarkii) via regulating PI3K/Akt/NF-κB pathway

Selenium (Se), an indispensable micronutrient for living organisms, has been extensively studied for its heavy metal-detoxifying properties in diverse biological systems and tissues. Nevertheless, it is not entirely certain whether Se can effectively protect against Cadmium (Cd)-induced gut inflammation, especially in aquatic animals. In this study, we employed various approaches, including transcriptome profiling, histological examinations, assessment of antioxidant enzyme activities, and analysis of gut microbiota composition to investigate the effects on crayfish growth and intestinal health after exposure to dietary Cd (15 mg kg−1 diet) and Se (15 mg kg−1 diet) individually or in combination for 8 weeks. The results revealed that dietary Cd exposure resulted in reduced body weight and survival rates, along with an increased occurrence of intestinal inflammation. Nevertheless, Se supplementation proved effective in mitigating the adverse effects of Cd on growth and gut health. Se exhibited a remarkable ability to counteract the disruption of gut antioxidant abilities induced by dietary Cd, as evidenced by the observed increases in ROS and MDA contents, decrease in GSH levels, and inhibition of antioxidative enzyme activities. At the concentration of 6 mg kg−1 in the diet, Se was found beneficial for maintaining gut microbiota richness and diversity. Among them, Flavobacterium, Thermomonas, and Chloronema displayed a weak negative correlation with the rate of gut inflammation. Meanwhile, the levels of short chain fatty acids (SCFAs), including acetic acid (AA) and butanoic acid (BA), showed a significant increase in the Se–Cd group compared to the Cd-only group. Furthermore, transcriptome analysis exhibited significant responses of the PI3K/Akt and NF-κB pathways following crayfish exposure to dietary Se and Cd, either separately or in combination. In short, this study provides a new evidence regarding the molecular mechanisms through which Se could regulate the PI3K/Akt and NF-κB pathways, either directly or indirectly via ROS and SCFAs, thereby alleviating Cd-induced gut inflammation in crayfish.

Evaluation of Prebiotic Activity of Stellariae Radix Polysaccharides and Its Effects on Gut Microbiota.

This study aims to evaluate the prebiotic potential of polysaccharides derived from Stellariae Radix (SRPs) and explore their influence on the gut microbiota composition in mice. Lactobacillus acidophilus and Bifidobacterium longum were cultivated in an MRS medium, while their growth kinetics, clumping behavior, sugar utilization, pH variation, growth density, and probiotic index were meticulously monitored. Additionally, the impact of crude Stellariae Radix polysaccharides (CSRP) on the richness and diversity of gut microbiota in mice was assessed via 16S rDNA sequencing. The results demonstrated the remarkable ability of CSRPs to stimulate the proliferation of Lactobacillus acidophilus and Bifidobacterium longum. Moreover, the oral administration of CSRPs to mice led to a noticeable increase in beneficial bacterial populations and a concurrent decrease in detrimental bacterial populations within the intestinal flora. These findings provided an initial validation of CSRPs as a promising agent in maintaining the equilibrium of gut microbiota in mice, thereby offering a substantial theoretical foundation for developing Stellariae Radix as a prebiotic ingredient in various applications, including food, healthcare products, and animal feed. Furthermore, this study presented novel insights for the exploration and utilization of Stellariae Radix resources.

Prickly Ash Seeds improve immunity of Hu sheep by changing the diversity and structure of gut microbiota.

Prickly Ash Seeds (PAS), as a traditional Chinese medicinal herb, have pharmacological effects such as anti-asthma, anti-thrombotic, and anti-bacterial, but their impact on gut microbiota is still unclear. This study used a full-length 16 s rRNA gene sequencing technique to determine the effect of adding PAS to the diet on the structure and distribution of gut microbiota in Hu sheep. All lambs were randomly divided into two groups, the CK group was fed with a basal ration, and the LZS group was given a basal diet with 3% of PAS added to the ration. The levels of inflammatory factors (IL-10, IL-1β, and TNF-α) in intestinal tissues were measured by enzyme-linked immunosorbent assay (ELISA) for Hu sheep in the CK and LZS group. The results indicate that PAS can increase the diversity and richness of gut microbiota, and can affect the community composition of gut microbiota. LEfSe analysis revealed that Verrucomicrobiota, Kiritimatiella, WCHB 41, and uncultured_rumen_bacterium were significantly enriched in the LZS group. KEGG pathway analysis found that LZS was significantly higher than the CK group in the Excretory system, Folding, sorting and degradation, and Immune system pathways (p < 0.05). The results of ELISA assay showed that the level of IL-10 was significantly higher in the LZS group than in the CK group (p < 0.05), and the levels of TNF-α and IL-1β were significantly higher in the CK group than in the LZS group (p < 0.05). LEfSe analysis revealed that the dominant flora in the large intestine segment changed from Bacteroidota and Gammaproteobacteria to Akkermansiaceae and Verrucomicrobiae after PAS addition to Hu sheep lambs; the dominant flora in the small intestine segment changed from Lactobacillales and Aeriscardovia to Kiritimatiellae and WCHB1 41. In conclusion, the addition of PAS to sheep diets can increase the number and types of beneficial bacteria in the intestinal tract, improve lamb immunity, and reduce intestinal inflammation. It provides new insights into healthy sheep production.

Multiomics Revealed the Multi-Dimensional Effects of Late Sleep on Gut Microbiota and Metabolites in Children in Northwest China.

Background Sleep plays a pivotal role in children's mental and physical development and has been linked to the gut microbiota in animals and adults. However, the characteristics of the gut microbiota and metabolites and the relationship to late bedtimes in children remain unclear. Methods In total, 88 eligible children, aged from 3 to 8 years, were recruited and divided into two groups according to the bedtime collected by designed questionnaires (early, before 22:00: n = 48; late, after 22:00, n = 40). Stools and plasma samples were collected to examine the characteristics of the gut microbiota and metabolites by shotgun metagenomics and metabolomics. Results The richness and diversity of the gut microbiota in children with early bedtime were significantly increased compared with the late ones. Coprococcus, Collinsella, Akkermansia muciniphila, and Bifidobacterium adolescentis were significantly more abundant in children with early bedtime, while Bacteroides and Clostridium sp. CAG-253 were obviously enriched in the late ones. A total of 106 metabolic pathways, including biosynthesis of ribonucleotide, peptidoglycan, and amino acids, and starch degradation were enriched in children with early bedtime, while 42 pathways were abundant in those with late bedtime. Notably, more gut microbial metabolites were observed in children with late bedtime, which included aldehyde, ketones, esters, amino acids and their metabolites, benzene and substituted derivatives, bile acids, heterocyclic compounds, nucleotide and metabolites, organic acid and derivatives, sugars and acyl carnitine. In plasma, fatty amides, lipids, amino acids, metabolites, hormones, and related compounds were enriched in children with early bedtime, while bile acids were higher in children with late bedtime. Association studies revealed that the different microbial species were correlated with metabolites from gut microbiota and plasma. Conclusions The results of our study revealed that the gut microbiota diversity and richness, and metabolic pathways were significantly extensive in children with early bedtime, whereas the gut microbial metabolites were significantly decreased, which might be related to gut microbial differences.

Pronounced gut microbiota signatures in patients with JAK2V617F-positive essential thrombocythemia.

Essential thrombocythemia (ET) is part of the Philadelphia chromosome-negative myeloproliferative neoplasms. It is characterized by an increased risk of thromboembolic events and also to a certain degree hypermetabolic symptoms. The gut microbiota is an important initiator of hematopoiesis and regulation of the immune system, but in patients with ET, where inflammation is a hallmark of the disease, it is vastly unexplored. In this study, we compared the gut microbiota via amplicon-based 16S rRNA gene sequencing of the V3-V4 region in 54 patients with ET according to mutation status Janus-kinase 2 (JAK2V617F)-positive vs JAK2V617F-negative patients with ET, and in 42 healthy controls (HCs). Gut microbiota richness was higher in patients with ET (median-observed richness, 283.5; range, 75-535) compared with HCs (median-observed richness, 191.5; range, 111-300; P < 0.001). Patients with ET had a different overall bacterial composition (beta diversity) than HCs (analysis of similarities [ANOSIM]; R = 0.063, P = 0.004). Patients with ET had a significantly lower relative abundance of taxa within the Firmicutes phylum compared with HCs (51% vs 59%, P = 0.03), and within that phylum, patients with ET also had a lower relative abundance of the genus Faecalibacterium (8% vs 15%, P < 0.001), an important immunoregulative bacterium. The microbiota signatures were more pronounced in patients harboring the JAK2V617F mutation, and highly similar to patients with polycythemia vera as previously described. These findings suggest that patients with ET may have an altered immune regulation; however, whether this dysregulation is induced in part by, or is itself inducing, an altered gut microbiota remains to be investigated. IMPORTANCE Essential thrombocythemia (ET) is a cancer characterized by thrombocyte overproduction. Inflammation has been shown to be vital in both the initiation and progression of other myeloproliferative neoplasms, and it is well known that the gut microbiota is important in the regulation of our immune system. However, the gut microbiota of patients with ET remains uninvestigated. In this study, we characterized the gut microbiota of patients with ET compared with healthy controls and thereby provide new insights into the field. We show that the gut microbiota of patients with ET differs significantly from that of healthy controls and the patients with ET have a lower relative abundance of important immunoregulative bacteria. Furthermore, we demonstrate that patients with JAK2V617F-positive ET have pronounced gut microbiota signatures compared with JAK2V617F-negative patients. Thereby confirming the importance of the underlying mutation, the immune response as well as the composition of the microbiota.

Comparative analysis of gut microbiota between common (Macaca fascicularis fascicularis) and Burmese (M. f. aurea) long-tailed macaques in different habitats

The environment has an important effect on the gut microbiota—an essential part of the host’s health—and is strongly influenced by the dietary pattern of the host as these together shape the composition and functionality of the gut microbiota in humans and other animals. This study compared the gut microbiota of Macaca fascicularis fascicularis and M. f. aurea in mangrove and island populations using 16S rRNA gene sequencing on a nanopore platform to investigate the effect of the environment and/or diet. The results revealed that the M. f. fascicularis populations that received anthropogenic food exhibited a higher richness and evenness of gut microbiota than the M. f. aurea populations in different habitats. Firmicutes and Bacteroidetes were the two most abundant bacterial phyla in the gut microbiota of both these subspecies; however, the relative abundance of these phyla was significantly higher in M. f. aurea than in M. f. fascicularis. This variation in the gut microbiota between the two subspecies in different habitats mostly resulted from the differences in their diets. Moreover, the specific adaptation of M. f. aurea to different environments with a different food availability had a significant effect on their microbial composition.

Strontium Chloride Improves Reproductive Function and Alters Gut Microbiota in Male Rats.

Strontium (Sr) is an essential trace element in the human body and plays an important role in regulating male reproductive health. Recent studies have shown that gut flora plays a key role in maintaining spermatogenesis, as well as testicular health, through the gut-testis axis. At present, it is unclear whether gut microbiota can mediate the effects of Sr on sperm quality, and what the underlying mechanisms may be. We investigated the effects of different concentrations of strontium chloride (SrCl2) solutions (0, 50, 100, and 200 mg/kg BW) on reproductive function and gut microbiota in male Wistar rats (6-8 weeks, 250 ± 20 g). All the animals were euthanized after 37 days of treatment. The Sr-50 group significantly increased sperm concentration, sperm motility, and sperm viability in rats. After Sr treatment, serum and testicular testosterone (T) and Sr levels increased in a dose-dependent manner with increasing Sr concentration. At the same time, we also found that testicular marker enzymes (ACP, LDH) and testosterone marker genes (StAR, 3β-HSD, and Cyp11a1) increased significantly in varying degrees after Sr treatment, while serum NO levels decreased significantly in a dose-dependent manner. Further investigation of intestinal flora showed that SrCl2 affected the composition of gut microbiome, but did not affect the richness and diversity of gut microbiota. Sr treatment reduced the number of bacteria with negative effects on reproductive health, such as Bacteroidetes, Tenericutes, Romboutsia, Ruminococcaceae_UCG_014, Weissella, and Eubacterium_coprostanoligenes_group, and added bacteria with negative effects on reproductive health, such as Jeotgalicoccus. To further explore the Sr and the relationship between the gut microbiota, we conducted a Spearman correlation analysis, and the results showed that the gut microbiota was closely correlated with Sr content in serum and testicular tissue, sex hormone levels, and testicular marker enzymes. Additionally, gut microbiota can also regulate each other and jointly maintain the homeostasis of the body's internal environment. However, we found no significant correlation between intestinal flora and sperm quality in this study, which may be related to the small sample size of our 16S rDNA sequencing. In conclusion, the Sr-50 group significantly increased T levels and sperm quality, and improved the levels of testicular marker enzymes and testosterone marker genes in the rats. Sr treatment altered the gut flora of the rats. However, further analysis of the effects of gut microbiota in mediating the effects of SrCl2 on male reproductive function is needed. This study may improve the current understanding of the interaction between Sr, reproductive health, and gut microbiota, providing evidence for the development of Sr-rich foods and the prevention of male fertility decline.

Ameliorative effect of Lactobacillus plantarum CCFM8661 on oleic acid-induced acne: Integrated the gut microbiota link to the acne pathogenesis.

Acne vulgaris is an inflammatory disease of the pilosebaceous unit of the skin that has serious adverse effects on the physical and mental health of patients. Probiotics are extensively employed in dermatology and could be an alternative option for acne therapy. Here, we evaluated the effect of oral ingestion of live and inactivated Lactobacillus plantarum CCFM8661 on oleic acid-induced acne using a mouse model. Results found that live L. plantarum CCFM8661 suppressed the skin inflammation and serum hormone (insulin and testosterone) production in acne mice. Parallelly, live L. plantarum CCFM8661 effectively reduced the formation of skin lipids (TG and NEFA), and normalized the expression of skin lipid metabolism-related genes (PPRA-γ, SREBP-1c, ACCα, FASN, PPRA-α, ACOX1, HSL and ATGL). In comparison, inactivated L. plantarum CCFM8661 had no effect on skin inflammation or serum hormone secretion, but decreased the skin TG and normalized the expression of skin lipid metabolism-related genes (PPRA-γ, SREBP-1c, FASN and ATGL) in acne mice. Both live and inactivated L. plantarum CCFM8661 raised the richness of gut microbiota, reduced the ratio of Bacteroidetes: Firmicutes, and decreased the relative abundance of Staphylococcus in the feces of acne mice. Oral ingestion of L. plantarum CCFM8661, particularly live cells, could alleviate acne by suppressing skin inflammation, normalizing the metabolism of hormones and skin lipids, which may be achieved by improving the gut microbial ecosystem. This article is protected by copyright. All rights reserved.

Strain-level structure of gut microbiome showed potential association with cognitive function in major depressive disorder: A pilot study

BackgroundAlthough the association between gut microbiota and the pathogenesis of major depressive disorder (MDD) has been well studied, it is unclear whether gut microbiota affects cognitive function in patients with MDD. In this study, we explored the association between gut microbiota and cognitive function in MDD and its possible mechanisms. MethodsWe enrolled 57 patients with MDD and 30 healthy controls (HCs) and used 16S rRNA gene sequencing analysis and shotgun metagenomic sequencing analysis to determine gut microbial composition. ResultsThe richness and diversity of gut microbiota in patients with MDD were the same as those in HCs, but there were differences in the abundance of Bifidobacterium and Blautia. Compared with HCs, two strains (bin_32 and bin_55) were significantly increased, and one strain (bin_31) was significantly decreased in patients with MDD based on the strain-level meta-analysis. Time to complete the Stroop-C had significant negative correlations with bin_31 and bin_32. Bin_55 had significant negative correlations with time to complete the Stroop-C, time to complete the Stroop-CW, and repeated animal words in 60 s but significant positive correlations with correct answers in 120 s on the Stroop-CW. LimitationsThis study only tested the cognitive function of MDD in a small sample, which may have caused some bias. ConclusionsBased on our strain-level analysis, we found that gut microbiota may be associated with the pathogenesis of MDD and may have potential effects on cognitive function.

Comparison of 16S rRNA gene sequencing microbiota among children with serological IgE-mediated food hypersensitivity.

We hypothesized that specific food hypersensitivity (FH) in children is linked to specific gut microbiota. The aim of our study was to quantify and evaluate differences in gut microbial composition among children with different IgE-mediated FH. Children (n = 81) aged 18 to 36 months were enrolled, fecal samples of 57 children with FH and 24 healthy children were evaluated using next-generation sequencing. Individual microbial diversity and composition were analyzed via targeting the 16 S rRNA gene hypervariable V3-V5 regions. Children with IgE-mediated FH (in milk, egg white, soy) had significantly lower gut microbiota diversity and richness than healthy children. Children with IgE-mediated FH exhibited relatively high abundances of Firmicutes and relative underrepresentation of the phylum Bacteroidetes. We observed significant increases in relative abundances of Ruminococcaceae, Clostridiaceae, and Erysipelotrichaceae (p < 0.01, compared to control) in children with milk hypersensitivity and of Clostridiaceae and Erysipelotrichaceae (p < 0.01) in children with peanut hypersensitivity. We also found significant increases in the numbers of Clostridiaceae, Lachnospiraceae and Pasteurellaceae (p < 0.01) in children with egg white hypersensitivity. These findings identify early evidence of different gut microbiota development/ differentiation in children with food hypersensitivity. Specific food hypersensitivities may be associated with compositional changes in intestinal microbiota. These findings identify early evidence of different gut microbiota development/differentiation in children with food hypersensitivity. We built a gut microbial profile that could identify toddlers at risk for food hypersensitivity. Children with enriched Firmicutes (phylum) with partial different families may be associated with food hypersensitivity. Enriched family Clostridiaceae, Ruminococcaceae, Lachnospiraceae, or Erysipelotrichaceae in gut microbiota may be associated with specific food hypersensitivities (such as milk, egg white, peanut) in children.

Ketogenic diet ameliorates attention deficit hyperactivity disorder in rats via regulating gut microbiota.

Attention deficit hyperactivity disorder (ADHD) is a common mental behavioral disorder in children. Alterations in gut microbiota composition are associated with neurological disorders. We aimed to investigate whether a ketogenic diet (KD) can be an alternative therapy for ADHD by altering the gut microbiota. Male spontaneously hypertensive rats (SHR) and Wistar Kyoto (WKY) rats were randomly allocated to the normal diet (ND), methylphenidate (MPH), and KD groups. SHR in groups KD and MPH exhibited a significant increase in behavioral characteristics of ADHD, such as distance moved and immobility time. KD and MPH treatment led to a significant elevation in concentrations of 5-HT, AC, cAMP, and NE of brain tissue and the expression of DRD1, DAT, PKA, DARPP32, and cAMP at the protein level in WKY rats and SHR. KD and MPH significantly increased the richness and diversity of gut microbiota in SHR. The abundance of Ruminococcus_gauvreauii_group, Bacteroides, Bifidobacterium, and Blautia significantly increased, whereas that of Lactobacillus, Romboutsia, Facklamia, and Turicibacter significantly declined in the KD group compared with the ND group. The gut microbiota in the KD group of SHR mainly participated in amino acid metabolism- and sugar metabolism-related pathways. KD might alleviate behavioral disorders in ADHD by regulating gut microbiota. This study provides novel insights for the use of KD in treating ADHD.

Fndc5/irisin deficiency leads to dysbiosis of gut microbiota contributing to the depressive-like behaviors in mice

BackgroundDepression is one of the most common mental diseases and the leading cause of disability worldwide. A dysfunctional gut microbiota-brain axis is one of the main pathological bases of depression. Irisin, an exercise-related myokine, reduces depression-like behaviors and may guide the relief of depressive symptoms by exercise. However, its underlying mechanism remains unclear. MethodsFibronectin type III domain containing 5 (Fndc5)/Irisin was knocked out in male wide-type C57BL/6N mice using CRISPR-cas9. The depression and anxiety symptoms were examined in irisin knockout and control mice with or without chronic unpredictable mild stress by sucrose preference test (SPT), forced swimming test (FST), and tail suspension test (TST). Fecal microbiota was assessed by 16S rRNA sequencing and microbiota-related metabolites using liquid chromatography with tandem mass spectrometry. Differential metabolites were analyzed with the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. ResultsThe knockout mice showed anxiety- and depression-like behaviors and altered diversity and richness of gut microbiota. At the phylum level, these mice had decreased Firmicutes and increased Bacteroidota populations, while at the genus level, they exhibited a low relative abundance of Lactobacillus and Bifidobacterium. Moreover, knocking out of Irisin gene in these mice significantly reduced N-desmethyl-mifepristone (RU 42633) and elevated (-)-stercobilin levels. The KEGG results showed that the microbiota-related metabolites affected by irisin mainly clustered into arginine and proline metabolism and affected the mechanistic target of rapamycin kinase (mTOR) signaling pathway. ConclusionOur findings show that Fndc5/irisin deficiency causes depression in mice by inducing dysbiosis of gut microbiota and changes in microbiota-related metabolites.

Zanthoxylum bungeanum amides ameliorates nonalcoholic fatty liver via regulating gut microbiota and activating AMPK/Nrf2 signaling

Ethnopharmacological relevanceZanthoxylum bungeanum Maxim. (Rutaceae) is a known herbal medicine with various bioactivities, including anti-obesity, lipid-lowering, learning & memory improving and anti-diabetes, and amides in Z. bungeanum (AZB) are considered as the major active agents for its bioactivities. Aim of the studyThis research was carried out to uncover the anti-NAFL effect of AZB and its corresponding molecular mechanisms. MethodsThe central composite design-response surface methodology (CCD-RSM) was utilized to optimize the AZB extraction process, and the anti-NAFL effect of AZB was investigated on high fat diet (HFD) fed mice (HFD mice). The levels of ROS in liver tissues were determined using laser confocal microscopy with DCFH-DA probe staining, and anti-enzymes (such as HO-1, SOD, CAT & GSH-PX) and MDA in liver tissues were measured using commercial detecting kits. GC-MS was used to determine the short-chain fatty acids (SCFAs) contents in feces and blood of mice. 16S high-throughput sequencing, western blotting (WB) assay and immunofluorescence (IF) were used to explore the intestinal flora changes in mice and the potential mechanisms of AZB for treatment of NAFL. ResultsOur results showed AZB reduced body weight, alleviated liver pathological changes, reduced fat accumulation, and improved oxidative stress in HFD mice. In addition, we also found AZB improved OGTT and ITT, reduced TG, TC, LDL-C, whereas increased HDL-C in HFD mice. AZB increased total number of the species and interspecies kinship of gut microbiota and reduced the richness and diversity of gut microbiota in HFD mice. Moreover, AZB decreased the ratio of Firmicutes/Bacteroidota, whereas increased the abundance of Allobaculum, Bacteroides and Dubosiella in feces of HFD-fed mice. Furthermore, AZB increased the production of SCFAs, and up-regulated the phosphorylation of AMPK and increased the nuclear transcription of Nrf2 in liver of HFD mice. ConclusionCollectively, our results suggested AZB can improve NAFL, which could reduce body weight, reverse liver lesions and fat accumulation, improve oxidative stress in liver tissues of HFD mice. Furthermore, the mechanisms are related to increase of the abundance of high-producing bacteria for SCFAs (e.g. Allobaculum, Bacteroides and Dubosiella) to activate AMPK/Nrf2 signaling.

Protective Effects of Bacillus subtilis HH2 against Oral Enterotoxigenic Escherichia coli in Beagles.

This study evaluated the protective effect of Bacillus subtilis HH2 on beagles orally challenged with enterotoxigenic Escherichia coli (ETEC). We assessed the physiological parameters and the severity of diarrhea, as well as the changes in three serum immunoglobulins (IgG, IgA, and IgM), plasma diamine oxidase (DAO), D-lactate (D-LA), and the fecal microbiome. Feeding B. subtilis HH2 significantly reduced the severity of diarrhea after the ETEC challenge (p < 0.05) and increased serum levels of IgG, IgA, and IgM (p < 0.01). B. subtilis HH2 administration also reduced serum levels of DAO at 48 h after the ETEC challenge (p < 0.05), but no significant changes were observed in D-LA (p > 0.05). Oral ETEC challenge significantly reduced the richness and diversity of gut microbiota in beagles not pre-fed with B. subtilis HH2 (p < 0.05), while B. subtilis HH2 feeding and oral ETEC challenge significantly altered the gut microbiota structure of beagles (p < 0.01). Moreover, 14 days of B. subtilis HH2 feeding reduced the relative abundance of Deinococcus-Thermus in feces. This study reveals that B. subtilis HH2 alleviates diarrhea caused by ETEC, enhances non-specific immunity, reduces ETEC-induced damage to the intestinal mucosa, and regulates gut microbiota composition.

Huangqin Decoction ameliorates ulcerative colitis by regulating fatty acid metabolism to mediate macrophage polarization via activating FFAR4-AMPK-PPARα pathway.

Huangqin Decoction (HQD), a traditional Chinese medicine (TCM) formula chronicled in Shang Han Lun, is safe and effective for treatment of ulcerative colitis (UC). To investigate the effect of HQD against dextran sulfate sodium (DSS)-induced UC mice by regulating gut microbiota and metabolites, and further explore the mechanism of fatty acid metabolism on macrophage polarization. Based on 3% dextran sulfate sodium (DSS)-induced UC mice model, clinical symptoms observation (body weight, DAI, and colon length) and histological inspection were used to evaluate the efficacy of HQD and fecal microbiota transplantation (FMT) from HQD-treated mice. The gut microbiota and metabolites were detected by 16S rRNA sequencing and metabolomics analysis. The parameters of fatty acid metabolism, macrophage polarization, and FFAR1/FFAR4-AMPK-PPARα pathway were analyzed by immunofluorescence analysis, western blotting, and real-time PCR. Then, the effects of FFAR1 and FFAR4 on macrophage polarization were examined by agonists based on LPS-induced RAW264.7cell model. The results showed that FMT, like HQD, ameliorated UC by improving weight loss, restoring colon length, and reducing DAI scores and histopathological scores. Besides, HQD and FMT both enhanced the richness of gut microbiota, and modulated intestinal bacteria and metabolites to achieve a new balance. Untargeted metabolomics analysis revealed that fatty acids, especially long-chain fatty acids (LCFAs), dominated in HQD against DSS-induced UC by regulating the gut microenvironment. Further, FMT and HQD recovered the expression of fatty acid metabolism-related enzymes, and simultaneously activated FFAR1/FFAR4-AMPK-PPARα pathway but suppressed NF-κB pathway. Combined with cell experiment, HQD and FMT promoted macrophage polarization from M1 toward M2, which were well associated with anti-inflammatory cytokines and combined with the activated FFAR4. The mechanism of HQD against UC was related to regulating fatty acid metabolism to mediate M2 macrophage polarization by activating the FFAR4-AMPK-PPARα pathway.

Prenatal physical activity and the gut microbiota of pregnant women: results from a preliminary investigation.

To determine whether physical activity (PA), specifically meeting the recommended 150 minutes of moderate-intensity PA per week, is associated with gut microbiota composition in pregnant women. In an ongoing birth cohort study, questions from the Behavioral Risk Factor Surveillance System, which provides data on PA variables, were used to determine whether pregnant women met or exceeded the PA recommendations. To profile the composition of gut bacterial microbiota, 16S rRNA sequencing was performed on stool samples obtained from pregnant women. Differences in alpha diversity metrics (richness, Pielou's evenness, and Shannon's diversity) according to PA were determined using linear regression, whereas beta diversity relationships (Canberra and Bray-Curtis) were assessed using Permutational multivariate analysis of variance (PERMANOVA). Differences in relative taxon abundance were determined using DESeq2. The complete analytical sample included 23 women that were evaluated for both PA and 16S rRNA sequencing data (median age [Q1; Q3] = 30.5 [26.6; 34.0] years; 17.4% Black), and 11 (47.8%) met or exceeded the PA recommendations. Meeting or exceeding the PA recommendations during pregnancy was not associated with gut microbiota richness, evenness, or diversity, but it was related to distinct bacterial composition using both Canberra (p = 0.005) and Bray-Curtis (p = 0.022) distances. Significantly lower abundances of Bacteroidales, Bifidobacteriaceae, Lactobacillaceae, and Streptococcaceae were observed in women who met or exceeded the PA recommendations (all false discovery rates adjusted, p &lt; 0.02). Pregnant women who met or exceeded the PA recommendations showed altered gut microbiota composition. This study forms the basis for future studies on the impact of PA on gut microbiota during pregnancy.

Probiotic potential of Lactobacillus sakei L-7 in regulating gut microbiota and metabolism

A growing body of research suggests that gut microbiota is inextricably linked to host health and disease，so we are committed to finding more probiotic resources that are beneficial to human health. This study evaluated the probiotic properties of Lactobacillus sakei L-7 isolated from home-made sausages. The basic probiotic properties of L. sakei L-7 were evaluated through in vitro tests. The strain showed 89% viability after 7 h of digestion in simulating gastric and intestinal fluid. The hydrophobicity, self-aggregation and co-aggregation of L. sakei L-7 showed it had a strong adhesion ability. C57BL/6 J mice were fed L. sakei L-7 for 4 weeks. 16 S rRNA gene analysis indicated that intake of L. sakei L-7 increased the richness of gut microbiota and abundance of beneficial bacteria Akkermansia, Allobaculum and Parabacteroides. Metabonomics analysis revealed that beneficial metabolite gamma-aminobutyric acid and docosahexaenoic acid increased significantly. While the level of metabolite sphingosine and arachidonic acid significantly decreased. In addition, serum levels of inflammatory cytokines interleukin (IL)− 6 and tumor necrosis factor (TNF)-α were significantly decreased. The results suggested that L. sakei L-7 may promote gut health and reduce the occurrence of inflammatory response, it has the potential to become a probiotic.

Dynamic distribution of gut microbiota during Alzheimer's disease progression in a mice model.

Alzheimer's disease (AD) is an irreversible neurodegenerative disease that affects more than 44 million people worldwide. The pathogenic mechanisms of AD still remain unclear. Currently, there are numerous studies investigating the microbiota-gut-brain axis in humans and rodents indicated that gut microbiota played a role in neurodegenerative diseases, including AD. However, the underlying relationship between the progress of AD disease and the dynamic distribution of gut microbiota is not well understood. In the present study, APPswe /PS1ΔE9 transgenic mice of different ages and sex were employed. After the evaluation of the AD mice model, gut metagenomic sequencing was conducted to reveal gut microbiota, moreover, probiotics intervention was treated in the AD mice. The results showed that (1) AD mice had reduced microbiota richness and a changed gut microbiota composition, and AD mice gut microbiota richness was correlated with cognitive performance. We have also found some potential AD-related microbes, for example, in AD-prone mice, the genus Mucispirillum was strongly associated with immune inflammation. (2) Probiotics intervention improved cognitive performance and changed gut microbiota richness and composition of AD mice. We revealed the dynamics distribution of gut microbiota and the effect of probiotics on AD in a mice model, which provides an important reference for the pathogenesis of AD, intestinal microbial markers associated with AD, and AD probiotic intervention.

Evaluation of the microbiota-sparing properties of the anti-staphylococcal antibiotic afabicin.

Antibiotic use is associated with collateral damage to the healthy microbiota. Afabicin is a first-in-class prodrug inhibitor of the FabI enzyme that, when converted to the pharmacologically active agent afabicin desphosphono, demonstrates a staphylococcal-specific spectrum of activity. An expected benefit of highly targeted antibiotics such as afabicin is microbiome preservation. To compare the effects of oral treatment with afabicin and standard-of-care antibiotics upon the murine gut microbiota, and to assess the effects of oral afabicin treatment on the human gut microbiota. Gut microbiota effects of a 10 day oral course of afabicin treatment were monitored in mice and compared with clindamycin, linezolid and moxifloxacin at human-equivalent dose levels using 16S rDNA sequencing. Further, the gut microbiota of healthy volunteers was longitudinally assessed across 20 days of oral treatment with afabicin 240 mg twice daily. Afabicin treatment did not significantly alter gut microbiota diversity (Shannon H index) or richness (rarefied Chao1) in mice. Only limited changes to taxonomic abundances were observed in afabicin-treated animals. In contrast, clindamycin, linezolid and moxifloxacin each caused extensive dysbiosis in the murine model. In humans, afabicin treatment was not associated with alterations in Shannon H or rarefied Chao1 indices, nor relative taxonomic abundances, supporting the findings from the animal model. Oral treatment with afabicin is associated with preservation of the gut microbiota in mice and healthy subjects.