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  • 1
    Online Resource
    Online Resource
    Epigallocatechin-3-Gallate Improves Intestinal Gut Microbiota Homeostasis and Ameliorates Clostridioides difficile Infection
    MDPI AG ; 2022
    In:  Nutrients Vol. 14, No. 18 ( 2022-09-11), p. 3756-
    Details
    In: Nutrients, MDPI AG, Vol. 14, No. 18 ( 2022-09-11), p. 3756-
    Abstract: Clostridioides difficile infection is closely related to the intestinal flora disorders induced by antibiotics, and changes in the intestinal flora may cause the occurrence and development of Clostridioides difficile infection. Epigallocatechin-3-gallate (EGCG) is one of the major bioactive ingredients of green tea and has been suggested to alleviate the growth of C. difficile in vitro. EGCG can ameliorate several diseases, such as obesity, by regulating the gut microbiota. However, whether EGCG can attenuate C. difficile infection by improving the gut microbiota is unknown. After establishing a mouse model of C. difficile infection, mice were administered EGCG (25 or 50 mg/kg/day) or PBS intragastrically for 2 weeks to assess the benefits of EGCG. Colonic pathology, inflammation, the intestinal barrier, gut microbiota composition, metabolomics, and the transcriptome were evaluated in the different groups. Compared with those of the mice in the CDI group, EGCG improved survival rates after infection, improved inflammatory markers, and restored the damage to the intestinal barrier. Furthermore, EGCG could improve the intestinal microbial community caused by C. difficile infection, such as by reducing the relative abundance of Enterococcaceae and Enterobacteriaceae. Moreover, EGCG can increase short-chain fatty acids, improve amino acid metabolism, and downregulate pathways related to intestinal inflammation. EGCG alters the microbiota and alleviates C. difficile infection, which provides new insights into potential therapies.
    Type of Medium: Online Resource
    ISSN: 2072-6643
    URL: Article
    DOI: 10.3390/nu14183756
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2518386-2
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  • 2
    Online Resource
    Online Resource
    Bifidobacterium longum R0175 Protects Rats against d -Galactosamine-Induced Acute Liver Failure
    American Society for Microbiology ; 2020
    In:  mSphere Vol. 5, No. 1 ( 2020-02-26)
    Details
    In: mSphere, American Society for Microbiology, Vol. 5, No. 1 ( 2020-02-26)
    Abstract: Acute liver failure is a severe liver disorder that poses considerable global challenges. Previous studies on Bifidobacterium longum R0175 have mainly focused on its psychotropic functions. The current research focused on the protective efficacy of B. longum R0175 against acute liver failure caused by d -galactosamine ( d -GalN) in rats and further tested the hypothesis that B. longum R0175 exerted liver-protective effects by affecting the intestinal microbiota and fecal metabolites and by inhibiting inflammation. We found that oral gavage of B. longum R0175 markedly reduced the severity of liver injury in d -GalN-treated rats, as evidenced by decreased serum levels of aspartate aminotransferase (AST) and total bile acids (TBAs) ( P 〈 0.05). Moreover, the plasma concentrations of proinflammatory cytokines (interleukin 1β [IL-1β] and tumor necrosis factor-α [TNF-α] ) and chemokines (granulocyte-macrophage colony-stimulating factor [GM-CSF], macrophage chemoattractant protein 1 [MCP-1] , chemokine [C-X-C motif] ligand 1 [CXCL1] , chemokine [C-C motif] ligand 5 [CCL5] , and macrophage inflammatory protein-1α [MIP-1α]) were also markedly reduced ( P 〈 0.05). Pretreatment with B. longum R0175 partially reversed the gut microbiota dysbiosis in rats with liver injury by increasing the relative abundances of potentially beneficial bacteria, such as Alloprevotella spp., and decreasing the relative abundances of potentially harmful bacteria, such as Acetatifactor muris , Butyricimonas spp., and Oscillibacter spp. Furthermore, B. longum R0175 administration partially improved the metabolic function of the intestinal microbes, as indicated by the decreased level of lithocholic acid found in the feces. IMPORTANCE Our research investigated the protective and preventive roles of B. longum R0175 in a rat model of acute liver failure. The results illustrated that this probiotic strain exhibited protective effects in rats with acute liver failure. Thus, B. longum R0175 showed clinical application prospects that required further exploration.
    Type of Medium: Online Resource
    ISSN: 2379-5042
    URL: Article
    DOI: 10.1128/mSphere.00791-19
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2020
    detail.hit.zdb_id: 2844248-9
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  • 3
    Online Resource
    Online Resource
    Bifidobacterium longum R0175 protects mice against APAP-induced liver injury by modulating the Nrf2 pathway
    Elsevier BV ; 2023
    In:  Free Radical Biology and Medicine Vol. 203 ( 2023-07), p. 11-23
    Details
    In: Free Radical Biology and Medicine, Elsevier BV, Vol. 203 ( 2023-07), p. 11-23
    Type of Medium: Online Resource
    ISSN: 0891-5849
    URL: Article
    DOI: 10.1016/j.freeradbiomed.2023.03.026
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 1483653-1
    SSG: 12
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  • 4
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    DataSheet_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Cellular and Infection Microbiology Vol. 12 ( 2022-11-9)
    Details
    In: Frontiers in Cellular and Infection Microbiology, Frontiers Media SA, Vol. 12 ( 2022-11-9)
    Abstract: Diets rich in fiber may provide health benefits and regulate the gut microbiome, which affects the immune system. However, the role of dietary fiber in Clostridioides difficile infection (CDI) is controversial. Here, we investigated the use of fermentable fibers, such as inulin or pectin, to replace the insoluble fiber cellulose to explore how dietary fiber affects C. difficile -induced colitis in mice through intestinal microecology and metabolomics. Using C. difficile VPI 10463, we generated a mouse model of antibiotic-induced CDI. We evaluated disease outcomes and the microbial community among mice fed two fermentable fibers (inulin or pectin) versus the insoluble fiber cellulose. We analyzed and compared the gut microbiota, intestinal epithelium, cytokine levels, immune responses, and metabolites between the groups. Severe histological injury and elevated cytokine levels were observed in colon tissues after infection. Different diets showed different effects, and pectin administration protected intestinal epithelial permeability. Pectin also steadily increased the diversity of the microbiome and decreased the levels of C. difficile -induced markers of inflammation in serum and colonic tissues. The pectin group showed a higher abundance of Lachnospiraceae and a lower abundance of the conditionally pathogenic Enterobacteriaceae than the cellulose group with infection. The concentration of short-chain fatty acids in the cecal contents was also higher in the pectin group than in the cellulose group. Pectin exerted its effects through the aryl hydrocarbon receptor (AhR) pathway, which was confirmed by using the AhR agonist FICZ and the inhibitor CH2223191. Our results show that pectin alters the microbiome and metabolic function and triggers a protective immune response.
    Type of Medium: Online Resource
    ISSN: 2235-2988
    URL: Article
    URL: Article
    DOI: 10.3389/fcimb.2022.1028267
    DOI: 10.3389/fcimb.2022.1028267.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2619676-1
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  • 5
    Online Resource
    Online Resource
    Administration of Bifidobacterium bifidum CGMCC 15068 modulates gut microbiota and metabolome in azoxymethane (AOM)/dextran sulphate sodium (DSS)-induced colitis-associated colon cancer (CAC) in mice
    Springer Science and Business Media LLC ; 2020
    In:  Applied Microbiology and Biotechnology Vol. 104, No. 13 ( 2020-07), p. 5915-5928
    Details
    In: Applied Microbiology and Biotechnology, Springer Science and Business Media LLC, Vol. 104, No. 13 ( 2020-07), p. 5915-5928
    Type of Medium: Online Resource
    ISSN: 0175-7598 , 1432-0614
    URL: Article
    DOI: 10.1007/s00253-020-10621-z
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 1464336-4
    SSG: 12
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  • 6
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    Multi-omic profiling reveals associations between the gut mucosal microbiome, the metabolome, and host DNA methylation associated gene expression in patients with colorectal cancer
    Springer Science and Business Media LLC ; 2020
    In:  BMC Microbiology Vol. 20, No. S1 ( 2020-04)
    Details
    In: BMC Microbiology, Springer Science and Business Media LLC, Vol. 20, No. S1 ( 2020-04)
    Abstract: The human gut microbiome plays a critical role in the carcinogenesis of colorectal cancer (CRC). However, a comprehensive analysis of the interaction between the host and microbiome is still lacking. Results We found correlations between the change in abundance of microbial taxa, butyrate-related colonic metabolites, and methylation-associated host gene expression in colonic tumour mucosa tissues compared with the adjacent normal mucosa tissues. The increase of genus Fusobacterium abundance was correlated with a decrease in the level of 4-hydroxybutyric acid (4-HB) and expression of immune-related peptidase inhibitor 16 ( PI16 ), Fc Receptor Like A ( FCRLA ) and Lymphocyte Specific Protein 1 ( LSP1 ). The decrease in the abundance of another potentially 4-HB-associated genus, Prevotella 2, was also found to be correlated with the down-regulated expression of metallothionein 1 M ( MT1M ). Additionally, the increase of glutamic acid-related family Halomonadaceae was correlated with the decreased expression of reelin ( RELN ). The decreased abundance of genus Paeniclostridium and genus Enterococcus were correlated with increased lactic acid level, and were also linked to the expression change of Phospholipase C Beta 1 ( PLCB1 ) and Immunoglobulin Superfamily Member 9 ( IGSF9 ) respectively. Interestingly, 4-HB, glutamic acid and lactic acid are all butyrate precursors, which may modify gene expression by epigenetic regulation such as DNA methylation. Conclusions Our study identified associations between previously reported CRC-related microbial taxa, butyrate-related metabolites and DNA methylation-associated gene expression in tumour and normal colonic mucosa tissues from CRC patients, which uncovered a possible mechanism of the role of microbiome in the carcinogenesis of CRC. In addition, these findings offer insight into potential new biomarkers, therapeutic and/or prevention strategies for CRC.
    Type of Medium: Online Resource
    ISSN: 1471-2180
    URL: Article
    DOI: 10.1186/s12866-020-01762-2
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2041505-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Western Diet Aggravated Carbon Tetrachloride‐Induced Chronic Liver Injury by Disturbing Gut Microbiota and Bile Acid Metabolism
    Wiley ; 2021
    In:  Molecular Nutrition & Food Research Vol. 65, No. 7 ( 2021-04)
    Details
    In: Molecular Nutrition & Food Research, Wiley, Vol. 65, No. 7 ( 2021-04)
    Abstract: The high‐fat, high‐sucrose, and low‐fiber Western diet (WD) is popular in many countries and affects the onset and progression of many diseases. This study is aimed to explore the influence of the WD on chronic liver disease (CLD) and its possible mechanism. Methods and results C57BL/6 mice are given a control diet (CD) or WD and CLD is induced by intraperitoneally injecting carbon tetrachloride (CCL 4 ) twice a week for 8 weeks. The WD aggravated CCL 4 ‐induced chronic liver injury, as evidenced by increased serum transaminase levels, worsened hepatic inflammatory response, and fibrosis. Gut microbiota is disturbed in mice treated with CCL 4 +WD (WC group), manifested as the accumulation of Fusobacteria, Streptococcaceae , Streptococcus , Fusobacterium , and Prevotella and the depletion of Firmicutes , Lachnospiraceae , and Roseburia . Additionally, increased hepatic taurocholic acid in the WC group activated sphingosine‐1‐phosphate receptor 2, which is positively correlated with hepatic fibrosis and inflammation parameters. Mice in the WC group have higher fecal primary bile acid (BA) levels and lower fecal secondary/primary BA ratios. Serum FGF15 levels are also elevated in the WC group, which is positively correlated with hepatic inflammation. Conclusion WD accelerates the progression of CLD which is associated with changes in the gut microbiota and BA metabolism.
    Type of Medium: Online Resource
    ISSN: 1613-4125 , 1613-4133
    URL: Issue
    URL: Article
    DOI: 10.1002/mnfr.v65.7
    DOI: 10.1002/mnfr.202000811
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2160372-8
    SSG: 12
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  • 8
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    Table_1.DOCX
    Frontiers Media SA ; 2022
    In:  Frontiers in Microbiology Vol. 13 ( 2022-5-18)
    Details
    In: Frontiers in Microbiology, Frontiers Media SA, Vol. 13 ( 2022-5-18)
    Abstract: Clostridioides difficile is a common cause of nosocomial infection. Antibiotic-induced dysbiosis in the intestinal microbiota is a core cause of C. difficile infection (CDI). Akkermansia muciniphila plays an active role in maintaining gastrointestinal balance and might offer the protective effects on CDI as probiotics. Here, we investigated the effects and mechanisms of A. muciniphila on CDI. C57BL/6 mice ( n = 29) were administered A. muciniphila Muc T (3 × 10 9 CFUs, 0.2 mL) or phosphate-buffered saline (PBS) by oral gavage for 2 weeks. Mice were pretreated with an antibiotic cocktail and subsequently challenged with the C. difficile strain VPI 10463. A. muciniphila treatment prevented weight loss in mice and reduced the histological injury of the colon. And it also alleviated inflammation and improved the barrier function of the intestine. The administration effects of A. muciniphila may be associated with an increase in short-chain fatty acid production and the maintenance of bile acids’ steady-state. Our results provide evidence that administration of A. muciniphila to CDI mice, with an imbalance in the microbial community structure, lead to a decrease in abundance of members of the Enterobacteriaceae and Enterococcaceae. In short, A. muciniphila shows a potential anti-CDI role by modulating gut microbiota and the metabolome.
    Type of Medium: Online Resource
    ISSN: 1664-302X
    URL: Article
    URL: Article
    DOI: 10.3389/fmicb.2022.841920
    DOI: 10.3389/fmicb.2022.841920.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2587354-4
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  • 9
    Online Resource
    Online Resource
    Ketogenic diet aggravates colitis, impairs intestinal barrier and alters gut microbiota and metabolism in DSS-induced mice
    Royal Society of Chemistry (RSC) ; 2021
    In:  Food & Function Vol. 12, No. 20 ( 2021), p. 10210-10225
    Details
    In: Food & Function, Royal Society of Chemistry (RSC), Vol. 12, No. 20 ( 2021), p. 10210-10225
    Abstract: Inflammatory bowel disease (IBD) is an idiopathic inflammatory disease with a high incidence. Multiple factors including dietary composition contribute to its occurrence. Recently, ketogenic diet which consists of a high proportion of fat and low carbohydrates has gained great popularity. Our study is aimed to explore the effect of ketogenic diet on IBD and its potential mechanisms. C57BL/6 mice were given a ketogenic diet or a control diet for a month and IBD was induced by 2% DSS in drinking water in the last week. Gut histology, inflammatory cytokines and chemokines, gut microbiota and metabolism were assessed. Ketogenic diet substantially worsened colitis, in terms of higher body weight loss, DAI scores and histological scores as well as colon length shortening. Levels of serum and colon inflammatory cytokines and chemokines (IL-1α, IL-6, TNF-α, IL-17, GM-CSF and IL-10) were significantly up-regulated in mice treated with ketogenic diet and DSS. Increased intestinal permeability and decreased expressions of intestinal epithelial barrier associated genes were observed due to ketogenic diet administration. Pretreatment with ketogenic diet alters the bacterial abundance, increasing pathogenic taxa such as Proteobacteria , Enterobacteriaceae , Helicobacter and Escherichia-Shigella and decreasing potential beneficial taxa such as Erysipelotrichaceae . Ketogenic diet also modified gut metabolism, increasing metabolites in the bile secretion such as ouabain, taurochenodeoxycholic acid, quinine, cholic acid and glycocholic acid, and decreasing metabolites associated with the biosynthesis of unsaturated fatty acids including stearic acid, arachidic acid, erucic acid, and docosanoic acid. These results suggest that ketogenic diet aggravates DSS-induced colitis in mice by increasing intestinal and systemic inflammation, and disrupting the intestinal barrier, which results from modulated gut microbiota and metabolism.
    Type of Medium: Online Resource
    ISSN: 2042-6496 , 2042-650X
    URL: Article
    DOI: 10.1039/D1FO02288A
    Language: English
    Publisher: Royal Society of Chemistry (RSC)
    Publication Date: 2021
    detail.hit.zdb_id: 2578152-2
    SSG: 21
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  • 10
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    Multi-Omics Analysis Reveals the Protection of Gasdermin D in Concanavalin A-Induced Autoimmune Hepatitis
    American Society for Microbiology ; 2022
    In:  Microbiology Spectrum Vol. 10, No. 5 ( 2022-10-26)
    Details
    In: Microbiology Spectrum, American Society for Microbiology, Vol. 10, No. 5 ( 2022-10-26)
    Abstract: Autoimmune hepatitis (AIH) is a progressive inflammation-associated liver injury. Pyroptosis is a novel inflammatory programmed cell death wherein gasdermin D (GSDMD) serves as the executioner. Our work challenged Gsdmd −/− mice with concanavalin A (ConA) to try to unveil the actual role of GSDMD in AIH. After ConA injection, Gsdmd −/− mice exhibited more severe liver damage characterized by a lower survival rate, more extensive hepatocyte necrosis and apoptosis, and higher serum transaminase levels, indicating the protection of GSDMD in ConA-induced AIH. Furthermore, the Gsdmd −/− mice exhibited higher hepatic expression and serum levels of inflammatory cytokines (gamma interferon [IFN-γ], tumor necrosis factor alpha [TNF-α] , and interleukin-17A [IL-17A]) and more infiltration of macrophages and neutrophils after ConA treatment than did wild-type (WT) mice. Gsdmd −/− mice with AIH showed increased hepatic l -glutamine levels but decreased glycerophospholipid metabolites levels. L-glutamine levels showed positive correlations while glycerophospholipid metabolites showed negative associations with liver injury indexes and inflammation markers. We further observed a destroyed intestinal barrier in Gsdmd −/− mice after ConA injection as indicated by decreased transcriptional expressions of Tjp1 , Ocln , Reg3g , and Muc2 . ConA-treated Gsdmd −/− mice also exhibited higher serum LPS binding protein (LBP) concentrations and hepatic Tlr4 and Cd14 mRNA levels. Further fecal 16S rRNA gene sequencing demonstrated decreased relative abundances of Lactobacillus and Roseburia but increased relative abundances of Allobaculum and Dubosiella in Gsdmd −/− mice with AIH. Lactobacillus was negatively correlated with liver injury and inflammation indexes and positively associated with Ocln , Muc2 , and Reg3g levels. Allobaculum was positively related to liver injury and inflammatory cytokines and negatively correlated with gut barrier indexes. IMPORTANCE Our study provides the first direct clues to the protective role of gasdermin D (GSDMD) in autoimmune hepatitis (AIH). We demonstrated that Gsdmd knockout exacerbated concanavalin A (ConA)-induced AIH in mice. It may be due to the destroyed intestinal barrier and changes in certain intestinal microbes and hepatic metabolites resulting in increased liver injury and inflammation in ConA-treated Gsdmd −/− mice. This finding suggested a nonnegligible role of GSDMD in AIH and also confirmed its physiological nonpyroptosis effects on the host. The role of GSDMD in autoimmune liver diseases or other liver diseases is complex and intriguing, deserving deep investigation.
    Type of Medium: Online Resource
    ISSN: 2165-0497
    URL: Article
    DOI: 10.1128/spectrum.01717-22
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2022
    detail.hit.zdb_id: 2807133-5
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