Roseburia intestinalis

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Xiaoyan Wang - One of the best experts on this subject based on the ideXlab platform.

  • Roseburia intestinalis derived flagellin ameliorates colitis by targeting mir 223 3p mediated activation of nlrp3 inflammasome and pyroptosis
    Molecular Medicine Reports, 2020
    Co-Authors: Shiyu Pan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Xiaoyan Wang
    Abstract:

    Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), which is a chronic, relapsing condition associated with the disorder of gut microbial communities. A previous study reported that levels of Roseburia intestinalis (R.I), a butyrate‑producing bacterium, are significantly decreased in patients with IBD and exert an anti‑inflammatory function in dextran sulfate sodium (DSS)‑induced colitis. However, the role of R.I flagellin in UC and its underlying molecular mechanism are not yet fully understood. Therefore, a DSS‑induced colitis model in C57Bl/6 mice and the LPS/ATP‑induced THP‑1 macrophages were treated with R.I flagellin, which were used to investigate the anti‑inflammatory effects of R.I flagellin. The results demonstrated that R.I flagellin decreased colitis‑associated disease activity index, colonic shortening and the pathological damage of the colon tissues in murine colitis models. Furthermore, R.I flagellin decreased the serum levels of proinflammatory cytokines and inhibited activation of the nucleotide‑binding oligomerization segment‑like receptor family 3 (NLRP3) inflammasome in murine colitis. R.I flagellin was also demonstrated to decrease the Gasdermin D to yield the N‑terminal fragment membrane pore and inhibit inflammasome‑triggered pyroptosis. In vitro analysis indicated that microRNA (miR)‑223‑3p was involved in the regulation of R.I flagellin on NLRP3 inflammasome activation. Taken together, the results of the present study demonstrated that R.I flagellin inhibited activation of the NLRP3 inflammasome and pyroptosis via miR‑223‑3p/NLRP3 signaling in macrophages, suggesting that R.I flagellin may be used as a novel probiotic product for the treatment of UC.

  • Roseburia intestinalis‑derived flagellin ameliorates colitis by targeting miR‑223‑3p‑mediated activation of NLRP3 inflammasome and pyroptosis.
    Molecular medicine reports, 2020
    Co-Authors: Shiyu Pan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Xiaoyan Wang
    Abstract:

    Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), which is a chronic, relapsing condition associated with the disorder of gut microbial communities. A previous study reported that levels of Roseburia intestinalis (R.I), a butyrate‑producing bacterium, are significantly decreased in patients with IBD and exert an anti‑inflammatory function in dextran sulfate sodium (DSS)‑induced colitis. However, the role of R.I flagellin in UC and its underlying molecular mechanism are not yet fully understood. Therefore, a DSS‑induced colitis model in C57Bl/6 mice and the LPS/ATP‑induced THP‑1 macrophages were treated with R.I flagellin, which were used to investigate the anti‑inflammatory effects of R.I flagellin. The results demonstrated that R.I flagellin decreased colitis‑associated disease activity index, colonic shortening and the pathological damage of the colon tissues in murine colitis models. Furthermore, R.I flagellin decreased the serum levels of proinflammatory cytokines and inhibited activation of the nucleotide‑binding oligomerization segment‑like receptor family 3 (NLRP3) inflammasome in murine colitis. R.I flagellin was also demonstrated to decrease the Gasdermin D to yield the N‑terminal fragment membrane pore and inhibit inflammasome‑triggered pyroptosis. In vitro analysis indicated that microRNA (miR)‑223‑3p was involved in the regulation of R.I flagellin on NLRP3 inflammasome activation. Taken together, the results of the present study demonstrated that R.I flagellin inhibited activation of the NLRP3 inflammasome and pyroptosis via miR‑223‑3p/NLRP3 signaling in macrophages, suggesting that R.I flagellin may be used as a novel probiotic product for the treatment of UC.

  • Roseburia intestinalis inhibits oncostatin M and maintains tight junction integrity in a murine model of acute experimental colitis.
    Scandinavian journal of gastroenterology, 2019
    Co-Authors: Bei Tan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Xiangrui Meng, Zhenyu Yang, Li Tian, Xiaoyan Wang
    Abstract:

    Objective: Levels of oncostatin M (OSM) and the composition of gut microbiota predict responses to anti-TNF agents used for IBD therapy. Here, the aim was to investigate the effects of Roseburia in...

  • insights into Roseburia intestinalis which alleviates experimental colitis pathology by inducing anti inflammatory responses
    Journal of Gastroenterology and Hepatology, 2018
    Co-Authors: Zhaohua Shen, Weiwei Luo, Bei Tan, Yongsheng Quan, Changxin Zhu, Zhenyu Yang, Jin-ming Yang, Wei Yuan, Xiaoyan Wang
    Abstract:

    BACKGROUND AND AIM The study aims to elucidate the anti-inflammatory effect and mechanism of Roseburia intestinalis (R. intestinalis) in Crohn's disease (CD). METHODS 16S-rRNA genome sequencing technique is used to detect the characteristics of intestinal microbiota in untreated CD patients and healthy controls. Then the study investigates the effects of R. intestinalis on disease activity index score, intestinal pathology, the differentiation of Treg cells, and the expressions of Thymic stromal lymphopoietin (TSLP), TGF-β and IL-10 by using TNBS colitis models. At the cellular level, the study uses LPS to stimulate Caco-2 cells to conduct inflammation models and then co-culture with R. intestinalis and detect changes of TSLP and TGF-β. The study then uses R. intestinalis to stimulate peripheral blood mononuclear cells, and the change of Treg cells was detected. RESULTS Genome sequencing of fecal samples from untreated CD patients (n = 10) revealed decreases in the abundance and diversity of intestinal microbiota, including R. intestinalis. Moreover, R. intestinalis reduced disease activity index scores, colon shortening, intestinal mucosal epithelial injury, and mucosal lymphocyte infiltration in a colitis mice model. It suppressed intestinal inflammation by increasing Treg cell numbers and expression of the anti-inflammatory cytokines TSLP, TGF-β, and interleukin-10 (P < 0.05). R. intestinalis also increased secretion of TSLP and TGF-β in lipopolysaccharide-treated Caco-2 cells. CONCLUSION These findings suggest that R. intestinalis suppresses CD pathogenesis by inducing anti-inflammatory responses.

  • Roseburia intestinalis inhibits interleukin 17 excretion and promotes regulatory t cells differentiation in colitis
    Molecular Medicine Reports, 2018
    Co-Authors: Changxin Zhu, Zhaohua Shen, Weiwei Luo, Bei Tan, Yongsheng Quan, Kerui Song, Zhenyu Yang, Kai Tang, Xiaoyan Wang
    Abstract:

    Roseburia intestinalis (R. intestinalis) is one of the dominant intestinal bacterial microbiota and is decreased in patients with inflammatory bowel disease (IBD). It helps protect colonic mucosa against the development of inflammation and subsequent IBD, however its underlying mechanisms are unclear. The aim of the present study was to evaluate the anti‑inflammatory properties of R. intestinalis in vitro and in an animal model of IBD. The effects of R. intestinalis on disease activity index (DAI) scores, intestinal pathology, the expression of interleukin (IL)‑17 and the frequency of CD4+CD25+Foxp3+ regulatory T cells (Treg) were evaluated in vivo in a model of 2,4,6‑trinitrobenzenesulfonic acid solution (TNBS)‑induced colitis. Compared with the control group, TNBS‑treated mice had significantly higher secretion of IL‑17, higher DAI scores, a lower ratio of Treg, reduced colon lengths and higher histological scores for colon inflammation. The administration of R. intestinalis significantly downregulated the expression of IL‑17, increased the ratio of Treg and ameliorated the high DAI scores and the pathological signs of inflammation in the colon compared with mice treated with TNBS alone. Gene expression profiling was also used to detect the expression of IL‑17 in human IBD and healthy control specimens. To extend these findings to an in vitro model of inflammation the human colon epithelial cell line NCM460 was stimulated with lipopolysaccharide (LPS) to induce inflammation and co‑cultured with R. intestinalis and changes in IL‑17 expression were evaluated. R. intestinalis inhibited the LPS‑induced secretion of IL‑17 by NCM460 cells. In conclusion, these results demonstrate that R. intestinalis inhibits IL‑17 secretion and promotes Treg differentiation in colitis, suggesting that R. intestinalis could be of potential use in the treatment of IBD.

Sylvia H. Duncan - One of the best experts on this subject based on the ideXlab platform.

  • Circulating and Tissue-Resident CD4 + T Cells With Reactivity to Intestinal Microbiota Are Abundant in Healthy Individuals and Function Is Altered During Inflammation
    Gastroenterology, 2017
    Co-Authors: Ahmed N. Hegazy, Nathan R. West, Michael J. T. Stubbington, Emily Wendt, Kim I.m. Suijker, Angeliki Datsi, Sebastien This, Camille Danne, Suzanne Campion, Sylvia H. Duncan
    Abstract:

    Background & Aims Interactions between commensal microbes and the immune system are tightly regulated and maintain intestinal homeostasis, but little is known about these interactions in humans. We investigated responses of human CD4 + T cells to the intestinal microbiota. We measured the abundance of T cells in circulation and intestinal tissues that respond to intestinal microbes and determined their clonal diversity. We also assessed their functional phenotypes and effects on intestinal resident cell populations, and studied alterations in microbe-reactive T cells in patients with chronic intestinal inflammation. Methods We collected samples of peripheral blood mononuclear cells and intestinal tissues from healthy individuals (controls, n = 13−30) and patients with inflammatory bowel diseases (n = 119; 59 with ulcerative colitis and 60 with Crohn's disease). We used 2 independent assays (CD154 detection and carboxy-fluorescein succinimidyl ester dilution assays) and 9 intestinal bacterial species ( Escherichia coli, Lactobacillus acidophilus, Bifidobacterium animalis subsp lactis, Faecalibacterium prausnitzii, Bacteroides vulgatus, Roseburia intestinalis, Ruminococcus obeum, Salmonella typhimurium, and Clostridium difficile ) to quantify, expand, and characterize microbe-reactive CD4 + T cells. We sequenced T-cell receptor Vβ genes in expanded microbe-reactive T-cell lines to determine their clonal diversity. We examined the effects of microbe-reactive CD4 + T cells on intestinal stromal and epithelial cell lines. Cytokines, chemokines, and gene expression patterns were measured by flow cytometry and quantitative polymerase chain reaction. Results Circulating and gut-resident CD4 + T cells from controls responded to bacteria at frequencies of 40−4000 per million for each bacterial species tested. Microbiota-reactive CD4 + T cells were mainly of a memory phenotype, present in peripheral blood mononuclear cells and intestinal tissue, and had a diverse T-cell receptor Vβ repertoire. These cells were functionally heterogeneous, produced barrier-protective cytokines, and stimulated intestinal stromal and epithelial cells via interleukin 17A, interferon gamma, and tumor necrosis factor. In patients with inflammatory bowel diseases, microbiota-reactive CD4 + T cells were reduced in the blood compared with intestine; T-cell responses that we detected had an increased frequency of interleukin 17A production compared with responses of T cells from blood or intestinal tissues of controls. Conclusions In an analysis of peripheral blood mononuclear cells and intestinal tissues from patients with inflammatory bowel diseases vs controls, we found that reactivity to intestinal bacteria is a normal property of the human CD4 + T-cell repertoire, and does not necessarily indicate disrupted interactions between immune cells and the commensal microbiota. T-cell responses to commensals might support intestinal homeostasis, by producing barrier-protective cytokines and providing a large pool of T cells that react to pathogens.

  • Correspondence
    2013
    Co-Authors: Sylvia H. Duncan, Petra Louis, Harry J. Flint, Karen P. Scott, Thaddeus B. Stanton, Rustam I. Aminov
    Abstract:

    Seven recently cultured bacterial isolates, although similar in their 16S rRNA gene sequences to Roseburia intestinalis L1-82 T (DSM 14610 T), were not sufficiently related for inclusion within existing species, forming three separate clusters in a 16S rRNA gene phylogenetic tree. The isolates, which were obtained from human stools, were Gram-variable or Gram-negative, strictly anaerobic, slightly curved rods; cells from all strains measured approximately 0?561?5–5?0 mm and were motile. Two strains belonging to one cluster (A2-181 and A2-183 T) were the only strains that were able to grow on glycerol and that failed to grow on any of the complex substrates tested (inulin, xylan and amylopectin). Strains belonging to a second cluster (represented by M6/1 and M72/1 T) differed from the other isolates in their ability to grow on sorbitol. Isolates belonging to a third cluster (L1-83 and A2-194 T) were the only strains that failed to grow on xylose and that gave good growth on inulin (strains M6/1 and M72/1 T gave weak growth). All strains were net acetate utilizers. The DNA G+C contents of representative Roseburia strains A2-183 T, A2-194 T, M72/1 T and R. intestinalis L1-82 T were 47?4, 41?4, 42?0 and 42?6 mol%, respectively. Based on 16S rRNA gene sequence similarity, three novel Roseburia species are proposed, with the names Roseburia hominis sp. nov. (type strain A2-183 T =DSM 16839 T =NCIMB 14029 T), Roseburi

  • Commensal bacteria in health and disease.
    Virulence Mechanisms of Bacterial Pathogens Fourth Edition, 2007
    Co-Authors: Harry J. Flint, Petra Louis, Karen P. Scott, Sylvia H. Duncan
    Abstract:

    Commensal gut bacteria have received a small fraction of the research effort that has been accorded to pathogens. The importance of commensal bacteria for normal gut function and health is increasingly being recognized. These bacteria play crucial roles in the metabolism of dietary components and the supply of energy to the gut mucosa and other host tissues, and influence the gut environment. They provide protection against pathogens through effective competition for growth requirements and binding sites while also participating in genetic exchange. Analyses of 16S rRNA genes amplified from gut and fecal samples have demonstrated remarkable diversity within the microbial communities of the gastrointestinal tract. Lactate is produced by a wide range of commensal gut bacteria but is not normally detected at concentrations above 2 mM in the feces of healthy individuals, although it is detected at much higher concentrations in patients with ulcerative colitis. Several low- G+C-content gram-positive species, including Ruminococcus hydrogenotrophicus, have been shown to be acetogenic and can both consume hydrogen and supply acetate when in coculture with the butyrate producer Roseburia intestinalis. Bacterial attachment must play a key role in the colonization of insoluble substrates. The impact of diet on susceptibility to pathogen infection may therefore be exerted partly through the effects of diet on the balance of commensal species and metabolic activity, as discussed in this chapter. In addition, poor diet is considered to contribute to long-term gut disorders, including inflammatory bowel disease, irritable bowel syndrome, and colorectal cancer.

  • Proposal of Roseburia faecis sp. nov., Roseburia hominis sp. nov. and Roseburia inulinivorans sp. nov., based on isolates from human faeces.
    International Journal of Systematic and Evolutionary Microbiology, 2006
    Co-Authors: Sylvia H. Duncan, Petra Louis, Rustam Aminov, Karen P. Scott, Thaddeus B. Stanton, Harry J. Flint
    Abstract:

    Seven recently cultured bacterial isolates, although similar in their 16S rRNA gene sequences to Roseburia intestinalis L1-82T (DSM 14610T), were not sufficiently related for inclusion within existing species, forming three separate clusters in a 16S rRNA gene phylogenetic tree. The isolates, which were obtained from human stools, were Gram-variable or Gram-negative, strictly anaerobic, slightly curved rods; cells from all strains measured approximately 0.5×1.5–5.0 μm and were motile. Two strains belonging to one cluster (A2-181 and A2-183T) were the only strains that were able to grow on glycerol and that failed to grow on any of the complex substrates tested (inulin, xylan and amylopectin). Strains belonging to a second cluster (represented by M6/1 and M72/1T) differed from the other isolates in their ability to grow on sorbitol. Isolates belonging to a third cluster (L1-83 and A2-194T) were the only strains that failed to grow on xylose and that gave good growth on inulin (strains M6/1 and M72/1T gave weak growth). All strains were net acetate utilizers. The DNA G+C contents of representative Roseburia strains A2-183T, A2-194T, M72/1T and R. intestinalis L1-82T were 47.4, 41.4, 42.0 and 42.6 mol%, respectively. Based on 16S rRNA gene sequence similarity, three novel Roseburia species are proposed, with the names Roseburia hominis sp. nov. (type strain A2-183T=DSM 16839T=NCIMB 14029T), Roseburia inulinivorans sp. nov. (type strain A2-194T=DSM 16841T=NCIMB 14030T) and Roseburia faecis sp. nov. (type strain M72/1T=DSM 16840T=NCIMB 14031T).

  • Effects of Alternative Dietary Substrates on Competition between Human Colonic Bacteria in an Anaerobic Fermentor System
    Applied and environmental microbiology, 2003
    Co-Authors: Sylvia H. Duncan, Colin S. Stewart, Hermie J. M. Harmsen, Karen P. Scott, Alan G. Ramsay, Gjalt W. Welling, Harry J. Flint
    Abstract:

    Duplicate anaerobic fermentor systems were used to examine changes in a community of human fecal bacteria supplied with different carbohydrate energy sources. A panel of group-specific fluorescent in situ hybridization probes targeting 16S rRNA sequences revealed that the fermentors supported growth of a greater proportion of Bacteroides and a lower proportion of gram-positive anaerobes related to Faecalibacterium prausnitzii, Ruminococcus flavefaciens-Ruminococcus bromii, Eubacterium rectale-Clostridium coccoides, and Eubacterium cylindroides than the proportions in the starting fecal inoculum. Nevertheless, certain substrates, such as dahlia inulin, caused a pronounced increase in the number of bacteria related to R. flavefaciens-R. bromii and E. cylindroides. The ability of three strictly anaerobic, gram-positive bacteria to compete with the complete human fecal flora was tested in the same experiment by using selective plating to enumerate the introduced strains. The Roseburia-related strain A2-183(F) was able to grow on all substrates despite the fact that it was unable to utilize complex carbohydrates in pure culture, and it was assumed that this organism survived by cross-feeding. In contrast, Roseburia intestinalis L1-82(R) and Eubacterium sp. strain A2-194(R) survived less well despite the fact that they were able to utilize polysaccharides in pure culture, except that A2-194(R) was stimulated 100-fold by inulin. These results suggest that many low-G+C-content gram-positive obligate anaerobes may be selected against during in vitro incubation, although several groups were stimulated by inulin. Thus, considerable caution is necessary when workers attempt to predict the in vivo effects of probiotics and prebiotics from their effects in vitro.

Christophe Chassard - One of the best experts on this subject based on the ideXlab platform.

  • Iron Modulates Butyrate Production by a Child Gut Microbiota In Vitro
    mBio, 2015
    Co-Authors: Alexandra Dostal, Lea Bircher, Christophe Lacroix, Van Thanh Pham, Rainer Follador, Michael B. Zimmermann, Christophe Chassard
    Abstract:

    ABSTRACT The aim of this study was to investigate the effect of iron (Fe) availability on butyrate production in the complex bacterial ecosystem of the human gut. Hence, different Fe availabilities were mimicked in an in vitro colonic fermentation model (the polyfermenter intestinal model called PolyFermS) inoculated with immobilized gut microbiota from a child and in batch cultures of the butyrate producer Roseburia intestinalis. Shifts in the microbial community (16S rRNA sequencing and quantitative PCR), metabolic activity (high-performance liquid chromatography), and expression of genes involved in butyrate production were assessed. In the PolyFermS, moderate Fe deficiency resulted in a 1.4-fold increase in butyrate production and a 5-fold increase in butyryl-coenzyme A (CoA):acetate CoA-transferase gene expression, while very strong Fe deficiency significantly decreased butyrate concentrations and butyrate-producing bacteria compared with the results under normal Fe conditions. Batch cultures of R. intestinalis grown in a low-Fe environment preferentially produced lactate and had reduced butyrate and hydrogen production, in parallel with upregulation of the lactate dehydrogenase gene and downregulation of the pyruvate:ferredoxin-oxidoreductase gene. In contrast, under high-Fe conditions, R. intestinalis cultures showed enhanced butyrate and hydrogen production, along with increased expression of the corresponding genes, compared with the results under normal-Fe conditions. Our data reveal the strong regulatory effect of Fe on gut microbiota butyrate producers and on the concentrations of butyrate, which contributes to the maintenance of host gut health. IMPORTANCE Fe deficiency is one of the most common nutritional deficiencies worldwide and can be corrected by Fe supplementation. In this in vitro study, we show that environmental Fe concentrations in a continuous gut fermentation model closely mimicking a child9s gut microbiota strongly affect the composition of the gut microbiome and its metabolic activity, particularly butyrate production. The differential expression of genes involved in the butyrate production pathway under different Fe conditions and the enzyme cofactor role of Fe explain the observed modulation of butyrate production. Our data reveal that the level of dietary Fe reaching the colon affects the microbiome, and its essential function of providing the host with beneficial butyrate.

  • characterization of the xylan degrading microbial community from human faeces
    FEMS Microbiology Ecology, 2007
    Co-Authors: Christophe Chassard, Vanessa Goumy, Marion Leclerc, Christophe Delhomme, Annick Bernalierdonadille
    Abstract:

    In humans, plant cell wall polysaccharides represent an important source of dietary fibres that are digested by gut microorganisms. Despite the extensive degradation of xylan in the colon, the population structure and the taxonomy of the predominant bacteria involved in degradation of this polysaccharide have not been extensively explored. The objective of our study was to characterize the xylanolytic microbial community from human faeces, using xylan from different botanic origins. The xylanolytic population was enumerated at high level in all faecal samples studied. The predominant xylanolytic organisms further isolated (20 strains) were assigned to Roseburia and Bacteroides species. Some Bacteroides isolates corresponded to the two newly described species Bacteroides intestinalis and Bacteroides dorei. Other isolates were closely related to Bacteroides sp. nov., a cellulolytic bacterium recently isolated from human faeces. The remaining Bacteroides strains could be considered to belong to a new species of this genus. Roseburia isolates could be assigned to the species Roseburia intestinalis. The xylanase activity of the Bacteroides and Roseburia isolates was found to be higher than that of other gut xylanolytic species previously identified. Our results provide new insights to the diversity and activity of the human gut xylanolytic community. Four new xylan-degrading Bacteroides species were identified and the xylanolytic capacity of R. intestinalis was further shown.

  • H2 and acetate transfers during xylan fermentation between a butyrate-producing xylanolytic species and hydrogenotrophic microorganisms from the human gut.
    FEMS microbiology letters, 2006
    Co-Authors: Christophe Chassard, Annick Bernalier-donadille
    Abstract:

    The aim of this work was to investigate in vitro interrelationships during xylan fermentation between an H2 and butyrate-producing xylanolytic species recently isolated in our laboratory from human faeces and identified as Roseburia intestinalis and the H2-utilizing acetogen Ruminococcus hydrogenotrophicus or the methanogen Methanobrevibacter smithii. H2 transfer between M. smithii or Ru. hydrogenotrophicus and the xylanolytic species was evidenced, confirming the great potential of these H2-consuming microorganisms to reutilize fermentative H2 during fibre fermentation in the gut. In addition, acetate transfer was demonstrated between the xylanolytic Roseburia sp. and the acetogenic species, both metabolites transfers leading to butyric fermentation of oat xylan without production of H2.

  • H-2 and acetate transfers during xylan fermentation between a butyrate-producing xylanolytic species and hydrogenotrophic microorganisms from the human gut
    FEMS Microbiology Letters, 2006
    Co-Authors: Christophe Chassard, Annick Bernalier-donadille
    Abstract:

    The aim of this work was to investigate in vitro interrelationships during xylan fermentation between an H-2 and butyrate-producing xylanolytic species recently isolated in our laboratory from human faeces and identified as Roseburia intestinalis and the H-2-utilizing acetogen Ruminococcus hydrogenotrophicus or the methanogen Methanobrevibacter smithii. H-2 transfer between M. smithii or Ru. hydrogenotrophicus and the xylanolytic species was evidenced, confirming the great potential of these H-2-consuming microorganisms to reutilize fermentative H2 during fibre fermentation in the gut. In addition, acetate transfer was demonstrated between the xylanolytic Roseburia sp. and the acetogenic species, both metabolites transfers leading to butyric fermentation of oat xylan without production of H-2.

Zhaohua Shen - One of the best experts on this subject based on the ideXlab platform.

  • Roseburia intestinalis derived flagellin ameliorates colitis by targeting mir 223 3p mediated activation of nlrp3 inflammasome and pyroptosis
    Molecular Medicine Reports, 2020
    Co-Authors: Shiyu Pan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Xiaoyan Wang
    Abstract:

    Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), which is a chronic, relapsing condition associated with the disorder of gut microbial communities. A previous study reported that levels of Roseburia intestinalis (R.I), a butyrate‑producing bacterium, are significantly decreased in patients with IBD and exert an anti‑inflammatory function in dextran sulfate sodium (DSS)‑induced colitis. However, the role of R.I flagellin in UC and its underlying molecular mechanism are not yet fully understood. Therefore, a DSS‑induced colitis model in C57Bl/6 mice and the LPS/ATP‑induced THP‑1 macrophages were treated with R.I flagellin, which were used to investigate the anti‑inflammatory effects of R.I flagellin. The results demonstrated that R.I flagellin decreased colitis‑associated disease activity index, colonic shortening and the pathological damage of the colon tissues in murine colitis models. Furthermore, R.I flagellin decreased the serum levels of proinflammatory cytokines and inhibited activation of the nucleotide‑binding oligomerization segment‑like receptor family 3 (NLRP3) inflammasome in murine colitis. R.I flagellin was also demonstrated to decrease the Gasdermin D to yield the N‑terminal fragment membrane pore and inhibit inflammasome‑triggered pyroptosis. In vitro analysis indicated that microRNA (miR)‑223‑3p was involved in the regulation of R.I flagellin on NLRP3 inflammasome activation. Taken together, the results of the present study demonstrated that R.I flagellin inhibited activation of the NLRP3 inflammasome and pyroptosis via miR‑223‑3p/NLRP3 signaling in macrophages, suggesting that R.I flagellin may be used as a novel probiotic product for the treatment of UC.

  • Roseburia intestinalis‑derived flagellin ameliorates colitis by targeting miR‑223‑3p‑mediated activation of NLRP3 inflammasome and pyroptosis.
    Molecular medicine reports, 2020
    Co-Authors: Shiyu Pan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Xiaoyan Wang
    Abstract:

    Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), which is a chronic, relapsing condition associated with the disorder of gut microbial communities. A previous study reported that levels of Roseburia intestinalis (R.I), a butyrate‑producing bacterium, are significantly decreased in patients with IBD and exert an anti‑inflammatory function in dextran sulfate sodium (DSS)‑induced colitis. However, the role of R.I flagellin in UC and its underlying molecular mechanism are not yet fully understood. Therefore, a DSS‑induced colitis model in C57Bl/6 mice and the LPS/ATP‑induced THP‑1 macrophages were treated with R.I flagellin, which were used to investigate the anti‑inflammatory effects of R.I flagellin. The results demonstrated that R.I flagellin decreased colitis‑associated disease activity index, colonic shortening and the pathological damage of the colon tissues in murine colitis models. Furthermore, R.I flagellin decreased the serum levels of proinflammatory cytokines and inhibited activation of the nucleotide‑binding oligomerization segment‑like receptor family 3 (NLRP3) inflammasome in murine colitis. R.I flagellin was also demonstrated to decrease the Gasdermin D to yield the N‑terminal fragment membrane pore and inhibit inflammasome‑triggered pyroptosis. In vitro analysis indicated that microRNA (miR)‑223‑3p was involved in the regulation of R.I flagellin on NLRP3 inflammasome activation. Taken together, the results of the present study demonstrated that R.I flagellin inhibited activation of the NLRP3 inflammasome and pyroptosis via miR‑223‑3p/NLRP3 signaling in macrophages, suggesting that R.I flagellin may be used as a novel probiotic product for the treatment of UC.

  • A new colitis therapy strategy via the target colonization of magnetic nanoparticle-internalized Roseburia intestinalis
    Biomaterials science, 2019
    Co-Authors: Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Junbo Hong
    Abstract:

    The homeostasis process in the gut tissue of humans relies on intestinal bacteria. However, the intestine is a complex structural tissue with a huge superficial area, and thus the effective application of probiotics in the treatment of Crohn's disease (CD) is still challenging. Herein, we show the feasibility of probiotic target delivery and retention using magnetic iron oxide nanoparticle-internalized Roseburia intestinalis, which can be easily directed by a magnetic field in vitro and in vivo. Subsequently, the increased colonization of this core profitable flora not only resulted in a better therapy effect than traditional intragastric administration but also altered the bacterial composition, leading to a higher diversity in microbial taxa in rats with colitis. Our findings illustrate the exciting opportunities that nanotechnology offers for alternative strategies to modulate biological systems remotely and precisely, which represent a step towards the wireless magnetic manipulation of living biological entities in microbiology.

  • Roseburia intestinalis supernatant ameliorates colitis induced in mice by regulating the immune response
    Molecular medicine reports, 2019
    Co-Authors: Weiwei Luo, Mengwei Xiao, Zhaohua Shen, Bei Tan, Changxin Zhu, Zhenyu Yang, Minzi Deng, Li Tian
    Abstract:

    Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), has a complex etiology that may be associated with dysbiosis of the microbiota. Previously, our study revealed significant loss of Roseburia intestinalis from the gut of untreated patients with CD, and that R. intestinalis exerted anti‑inflammatory functions in TNBS‑induced colitis; however, the function of R. intestinalis supernatant is unknown. Therefore, LPS‑induced macrophages, including RAW264.7 macrophages and bone marrow‑derived macrophages were treated with R. intestinalis supernatant. The results indicated that R. intestinalis supernatant suppressed expression of interleukin (IL)‑6 and signal transducer and activator of transcription 3 (STAT3) by macrophages. Additionally, these findings were further verified in vivo in DSS‑ and TNBS‑induced mouse models of colitis. It was observed that R. intestinalis supernatant ameliorated IBD colitis by reducing the number of inflammatory macrophages and Th17 cells in the colon, and by downregulating the expression of IL‑6 and STAT3. Finally, the non‑protein components of R. intestinalis supernatant were examined using gas chromatography‑mass spectrometry analysis and identified the presence of short‑chain fatty acids. In conclusion, the results of the present study indicated that R. intestinalis supernatant may regulate immune responses and ameliorate colitis.

  • Roseburia intestinalis inhibits oncostatin M and maintains tight junction integrity in a murine model of acute experimental colitis.
    Scandinavian journal of gastroenterology, 2019
    Co-Authors: Bei Tan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Xiangrui Meng, Zhenyu Yang, Li Tian, Xiaoyan Wang
    Abstract:

    Objective: Levels of oncostatin M (OSM) and the composition of gut microbiota predict responses to anti-TNF agents used for IBD therapy. Here, the aim was to investigate the effects of Roseburia in...

Bei Tan - One of the best experts on this subject based on the ideXlab platform.

  • Roseburia intestinalis derived flagellin ameliorates colitis by targeting mir 223 3p mediated activation of nlrp3 inflammasome and pyroptosis
    Molecular Medicine Reports, 2020
    Co-Authors: Shiyu Pan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Xiaoyan Wang
    Abstract:

    Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), which is a chronic, relapsing condition associated with the disorder of gut microbial communities. A previous study reported that levels of Roseburia intestinalis (R.I), a butyrate‑producing bacterium, are significantly decreased in patients with IBD and exert an anti‑inflammatory function in dextran sulfate sodium (DSS)‑induced colitis. However, the role of R.I flagellin in UC and its underlying molecular mechanism are not yet fully understood. Therefore, a DSS‑induced colitis model in C57Bl/6 mice and the LPS/ATP‑induced THP‑1 macrophages were treated with R.I flagellin, which were used to investigate the anti‑inflammatory effects of R.I flagellin. The results demonstrated that R.I flagellin decreased colitis‑associated disease activity index, colonic shortening and the pathological damage of the colon tissues in murine colitis models. Furthermore, R.I flagellin decreased the serum levels of proinflammatory cytokines and inhibited activation of the nucleotide‑binding oligomerization segment‑like receptor family 3 (NLRP3) inflammasome in murine colitis. R.I flagellin was also demonstrated to decrease the Gasdermin D to yield the N‑terminal fragment membrane pore and inhibit inflammasome‑triggered pyroptosis. In vitro analysis indicated that microRNA (miR)‑223‑3p was involved in the regulation of R.I flagellin on NLRP3 inflammasome activation. Taken together, the results of the present study demonstrated that R.I flagellin inhibited activation of the NLRP3 inflammasome and pyroptosis via miR‑223‑3p/NLRP3 signaling in macrophages, suggesting that R.I flagellin may be used as a novel probiotic product for the treatment of UC.

  • Roseburia intestinalis‑derived flagellin ameliorates colitis by targeting miR‑223‑3p‑mediated activation of NLRP3 inflammasome and pyroptosis.
    Molecular medicine reports, 2020
    Co-Authors: Shiyu Pan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Xiaoyan Wang
    Abstract:

    Ulcerative colitis (UC) is a type of inflammatory bowel disease (IBD), which is a chronic, relapsing condition associated with the disorder of gut microbial communities. A previous study reported that levels of Roseburia intestinalis (R.I), a butyrate‑producing bacterium, are significantly decreased in patients with IBD and exert an anti‑inflammatory function in dextran sulfate sodium (DSS)‑induced colitis. However, the role of R.I flagellin in UC and its underlying molecular mechanism are not yet fully understood. Therefore, a DSS‑induced colitis model in C57Bl/6 mice and the LPS/ATP‑induced THP‑1 macrophages were treated with R.I flagellin, which were used to investigate the anti‑inflammatory effects of R.I flagellin. The results demonstrated that R.I flagellin decreased colitis‑associated disease activity index, colonic shortening and the pathological damage of the colon tissues in murine colitis models. Furthermore, R.I flagellin decreased the serum levels of proinflammatory cytokines and inhibited activation of the nucleotide‑binding oligomerization segment‑like receptor family 3 (NLRP3) inflammasome in murine colitis. R.I flagellin was also demonstrated to decrease the Gasdermin D to yield the N‑terminal fragment membrane pore and inhibit inflammasome‑triggered pyroptosis. In vitro analysis indicated that microRNA (miR)‑223‑3p was involved in the regulation of R.I flagellin on NLRP3 inflammasome activation. Taken together, the results of the present study demonstrated that R.I flagellin inhibited activation of the NLRP3 inflammasome and pyroptosis via miR‑223‑3p/NLRP3 signaling in macrophages, suggesting that R.I flagellin may be used as a novel probiotic product for the treatment of UC.

  • A new colitis therapy strategy via the target colonization of magnetic nanoparticle-internalized Roseburia intestinalis
    Biomaterials science, 2019
    Co-Authors: Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Bei Tan, Xiangrui Meng, Kai Nie, Ting Tong, Junbo Hong
    Abstract:

    The homeostasis process in the gut tissue of humans relies on intestinal bacteria. However, the intestine is a complex structural tissue with a huge superficial area, and thus the effective application of probiotics in the treatment of Crohn's disease (CD) is still challenging. Herein, we show the feasibility of probiotic target delivery and retention using magnetic iron oxide nanoparticle-internalized Roseburia intestinalis, which can be easily directed by a magnetic field in vitro and in vivo. Subsequently, the increased colonization of this core profitable flora not only resulted in a better therapy effect than traditional intragastric administration but also altered the bacterial composition, leading to a higher diversity in microbial taxa in rats with colitis. Our findings illustrate the exciting opportunities that nanotechnology offers for alternative strategies to modulate biological systems remotely and precisely, which represent a step towards the wireless magnetic manipulation of living biological entities in microbiology.

  • Roseburia intestinalis supernatant ameliorates colitis induced in mice by regulating the immune response
    Molecular medicine reports, 2019
    Co-Authors: Weiwei Luo, Mengwei Xiao, Zhaohua Shen, Bei Tan, Changxin Zhu, Zhenyu Yang, Minzi Deng, Li Tian
    Abstract:

    Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), has a complex etiology that may be associated with dysbiosis of the microbiota. Previously, our study revealed significant loss of Roseburia intestinalis from the gut of untreated patients with CD, and that R. intestinalis exerted anti‑inflammatory functions in TNBS‑induced colitis; however, the function of R. intestinalis supernatant is unknown. Therefore, LPS‑induced macrophages, including RAW264.7 macrophages and bone marrow‑derived macrophages were treated with R. intestinalis supernatant. The results indicated that R. intestinalis supernatant suppressed expression of interleukin (IL)‑6 and signal transducer and activator of transcription 3 (STAT3) by macrophages. Additionally, these findings were further verified in vivo in DSS‑ and TNBS‑induced mouse models of colitis. It was observed that R. intestinalis supernatant ameliorated IBD colitis by reducing the number of inflammatory macrophages and Th17 cells in the colon, and by downregulating the expression of IL‑6 and STAT3. Finally, the non‑protein components of R. intestinalis supernatant were examined using gas chromatography‑mass spectrometry analysis and identified the presence of short‑chain fatty acids. In conclusion, the results of the present study indicated that R. intestinalis supernatant may regulate immune responses and ameliorate colitis.

  • Roseburia intestinalis inhibits oncostatin M and maintains tight junction integrity in a murine model of acute experimental colitis.
    Scandinavian journal of gastroenterology, 2019
    Co-Authors: Bei Tan, Mengwei Xiao, Zhaohua Shen, Weiwei Luo, Xiangrui Meng, Zhenyu Yang, Li Tian, Xiaoyan Wang
    Abstract:

    Objective: Levels of oncostatin M (OSM) and the composition of gut microbiota predict responses to anti-TNF agents used for IBD therapy. Here, the aim was to investigate the effects of Roseburia in...