Minor alterations in the intestinal microbiota composition upon Rotavirus infection do not affect susceptibility to DSS colitis.
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ABSTRACT:
SUBMITTER: Hamza KH
PROVIDER: S-EPMC8242028 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The aim of this study was to examine the effects of Lactobacillus brevis on the microbial community and serum metabolome in colitis induced by dextran sulfate sodium (DSS). ICR mice were randomly distributed into three treatment groups: (i) L. brevis treatment alone (control), (ii) DSS administration alone, and (iii) treatment with L. brevis and DSS. Our results demonstrate that L. brevis treatment significantly alleviated DSS-induced body weight loss and colon inflammation. In addition, LC-MS analysis of serum metabolites revealed that L. brevis treatment increased the serum level of metabolites against inflammatory responses or oxidative stressors caused by DSS in the murine model. By detecting colonic microbiota, L. brevis increased colonic microbial diversity after challenging with DSS, and increased the relative abundance of Alloprevotella at genus, but Bacteroidales was reduced (P < 0.05). These result indicated that L. brevis could lower the severity of colitis induced by DSS via improving reprogramming the serum metabolome and intestinal microbiota. These findings suggest that the probiotic L. brevis may prevent tissue damage from colitis.
| S-EPMC6759783 | biostudies-literature
Project description:BackgroundCompelling evidences demonstrated that gut microbiota dysbiosis plays a critical role in the pathogenesis of inflammatory bowel diseases (IBD). Therapies for targeting the microbiota may provide alternative options for the treatment of IBD, such as probiotics. Here, we aimed to investigate the protective effect of a probiotic strain, Pediococcus pentosaceus (P. pentosaceus) CECT 8330, on dextran sulfate sodium (DSS)-induced colitis in mice.MethodsC57BL/6 mice were administered phosphate-buffered saline (PBS) or P. pentosaceus CECT 8330 (5 × 108 CFU/day) once daily by gavage for 5 days prior to or 2 days after colitis induction by DSS. Weight, fecal conditions, colon length and histopathological changes were examined. ELISA and flow cytometry were applied to determine the cytokines and regulatory T cells (Treg) ratio. Western blot was used to examine the tight junction proteins (TJP) in colonic tissues. Fecal short-chain fatty acids (SCFAs) levels and microbiota composition were analyzed by targeted metabolomics and 16S rRNA gene sequencing, respectively. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and Cluster of orthologous groups of proteins (COG) pathway analysis were used to predict the microbial functional profiles.ResultsP. pentosaceus CECT 8330 treatment protected DSS-induced colitis in mice as evidenced by reducing the weight loss, disease activity index (DAI) score, histological damage, and colon length shortening. P. pentosaceus CECT 8330 decreased the serum levels of proinflammatory cytokines (TNF-α, IL-1β, and IL-6), and increased level of IL-10 in DSS treated mice. P. pentosaceus CECT 8330 upregulated the expression of ZO-1, Occludin and the ratio of Treg cells in colon tissue. P. pentosaceus CECT 8330 increased the fecal SCFAs level and relative abundances of several protective bacteria genera, including norank_f_Muribaculaceae, Lactobacillus, Bifidobacterium, and Dubosiella. Furthermore, the increased abundances of bacteria genera were positively correlated with IL-10 and SCFAs levels, and negatively associated with IL-6, IL-1β, and TNF-α, respectively. The KEGG and COG pathway analysis revealed that P. pentosaceus CECT 8330 could partially recover the metabolic pathways altered by DSS.ConclusionsP. pentosaceus CECT 8330 administration protects the DSS-induced colitis and modulates the gut microbial composition and function, immunological profiles, and the gut barrier function. Therefore, P. pentosaceus CECT 8330 may serve as a promising probiotic to ameliorate intestinal inflammation.
| S-EPMC8761308 | biostudies-literature
Project description:16S rRNA sequencing of human fecal samples has been tremendously successful in identifying microbiome changes associated with both aging and disease. A number of studies have described microbial alterations corresponding to physical frailty and nursing home residence among aging individuals. A gut-muscle axis through which the microbiome influences skeletal muscle growth/function has been hypothesized. However, the microbiome has yet to be examined in sarcopenia. Here, we collected fecal samples of 60 healthy controls (CON) and 27 sarcopenic (Case)/possibly sarcopenic (preCase) individuals and analyzed the intestinal microbiota using 16S rRNA sequencing. We observed an overall reduction in microbial diversity in Case and preCase samples. The genera Lachnospira, Fusicantenibacter, Roseburia, Eubacterium, and Lachnoclostridium-known butyrate producers-were significantly less abundant in Case and preCase subjects while Lactobacillus was more abundant. Functional pathways underrepresented in Case subjects included numerous transporters and phenylalanine, tyrosine, and tryptophan biosynthesis suggesting that protein processing and nutrient transport may be impaired. In contrast, lipopolysaccharide biosynthesis was overrepresented in Case and PreCase subjects suggesting that sarcopenia is associated with a pro-inflammatory metagenome. These analyses demonstrate structural and functional alterations in the intestinal microbiota that may contribute to loss of skeletal muscle mass and function in sarcopenia.
| S-EPMC7907362 | biostudies-literature
Project description:The intestinal microbiota is a complex ecosystem implicated in host health and disease. Inflammatory bowel disease (IBD) is a multifactorial chronic disorder of the gastrointestinal mucosa. Even though the exact mechanisms are still unknown, the intestinal microbiota is crucial in IBD development. We previously showed that murine norovirus (MNV) induces colitis in the Il10-deficient (Il10 -/-) mouse model of IBD in a microbiota-dependent manner. Thus, in this study we analyzed whether distinct minimal bacterial consortia influence the outcome of MNV-triggered colitis in Il10 -/- mice. Gnotobiotic Il10 -/- mice associated with Oligo-Mouse-Microbiota 12 (OMM12) or Altered Schaedler Flora (ASF) developed little to no inflammatory lesions in the colon and cecum. MNV infection exacerbated colitis severity only in ASF-colonized mice, but not in those associated with OMM12. Four weeks after MNV infection, inflammatory lesions in ASF-colonized Il10 -/- mice were characterized by epithelial hyperplasia, infiltration of inflammatory cells, and increased barrier permeability. Co-colonization of ASF-colonized Il10 -/- mice with segmented filamentous bacteria (SFB) abolished MNV-induced colitis, whereas histopathological scores in SFB-OMM12-co-colonized mice stayed unchanged. Moreover, SFB only colonized mice associated with ASF. The SFB-mediated protective effects in ASF-colonized mice involved enhanced activation of intestinal barrier defense mechanisms and mucosal immune responses in the chronic and acute phase of MNV infection. SFB colonization strengthened intestinal barrier function by increasing expression of tight junction proteins, antimicrobial peptides and mucus. Furthermore, SFB colonization enhanced the expression of pro-inflammatory cytokines such as Tnf?, Il1?, and Il12a, as well as the expression of the regulatory cytokine Tgf?. Altogether, our results showed that MNV-triggered colitis depends on the microbial context.
| S-EPMC6664081 | biostudies-literature
Project description:Gut microbiota is a complex aggregation of microbial organisms, which offers diverse protective benefits to the host. Dysbiosis of intestinal microbiota is frequently associated with many diseases. Vitamin D3 (VD), which was originally associated with bone health, also possesses antimicrobial activities and can act through antimicrobial peptide. Cathelicidin is a type of antimicrobial peptide in host to maintain the balance of gut microbiome. Our current study sought to evaluate the protective effect of VD and cathelicidin in mice intestines by administration of VD or mCRAMP-encoding L. lactis. We herein provided a comprehensive profile of the impact of VD and mCRAMP on gut microbiota using 16S rRNA sequencing, followed by bioinformatics and statistical analysis. Our results revealed an increased richness of bacterial community in mice intestines due to VD administration. Moreover, we showed a beneficial effect of VD and mCRAMP by enhancing the colonization of bacterial taxa that are associated with protective effects to the host but repressing the propagation of bacterial taxa that are associated with harmful effects to the host. Various metabolic pathways related to amino acid and lipid metabolism were affected in this process. We further established a bacterial panel as a reliable biomarker to evaluate the efficacy of remodeling the mice gut microbiota by VD and mCRAMP administration. The uncovered effects will deepen the comprehension about the antibacterial mechanisms of VD and mCRAMP and provide new insights for therapeutic implication of them.
| S-EPMC8732771 | biostudies-literature
Project description:Intestinal microbial dysbiosis contributes to the dysmetabolism of luminal factors, including steroid hormones (sterones) that affect the development of chronic gastrointestinal inflammation and the incidence of sterone-responsive cancers of the breast, prostate, and colon. Little is known, however, about the role of specific host sterone nucleoreceptors, including estrogen receptor ? (ER?), in microbiota maintenance. Herein, we test the hypothesis that ER? status affects microbiota composition and determine if such compositionally distinct microbiota respond differently to changes in diet complexity that favor Proteobacteria enrichment. To this end, conventionally raised female ER?(+/+) and ER?(-/-) C57BL/6J mice (mean age of 27 weeks) were initially reared on 8604, a complex diet containing estrogenic isoflavones, and then fed AIN-76, an isoflavone-free semisynthetic diet, for 2 weeks. 16S rRNA gene surveys revealed that the fecal microbiota of 8604-fed mice and AIN-76-fed mice differed, as expected. The relative diversity of Proteobacteria, especially the Alphaproteobacteria and Gammaproteobacteria, increased significantly following the transition to AIN-76. Distinct patterns for beneficial Lactobacillales were exclusive to and highly abundant among 8604-fed mice, whereas several Proteobacteria were exclusive to AIN-76-fed mice. Interestingly, representative orders of the phyla Proteobacteria, Bacteroidetes, and Firmicutes, including the Lactobacillales, also differed as a function of murine ER? status. Overall, these interactions suggest that sterone nucleoreceptor status and diet complexity may play important roles in microbiota maintenance. Furthermore, we envision that this model for gastrointestinal dysbiosis may be used to identify novel probiotics, prebiotics, nutritional strategies, and pharmaceuticals for the prevention and resolution of Proteobacteria-rich dysbiosis.
| S-EPMC3754184 | biostudies-literature
Project description:Algal oil is rich in docosahexaenoic acid (DHA) and has various health benefits against human metabolic disorders and disease. This study aimed to investigate the effects of DHA algal oil on colonic inflammation and intestinal microbiota in dextran sulfate sodium (DSS)-induced colitis mice model. Male C57BL/6 mice was induced colitis by 2.5% DSS and followed by 2 weeks of treatment with algal oil (250 or 500 mg/kg/day). The colonic inflammation was assessed by colon macroscopic damage scores, and the degree of neutrophil infiltration was evaluated by measuring tissue-associated myeloperoxidase (MPO) activity in colonic mucosa. Tight junction proteins in the colonic tissue were measured by real-time PCR and western blot. Moreover, the intestinal microbiota and shot chain fatty acids (SCFAs) were estimated by bioinformatic analysis and GC, respectively. Colonic damage due to DSS treatment was significantly ameliorated by algal oil supplementation. In addition, algal oil significantly inhibited the increases of malondialdehyde (MDA) content, MPO activity, pro-inflammatory cytokines level and tight junction proteins expression in DSS-treated mice. Furthermore, supplementation of algal oil modulated the intestinal microbiota structure in DSS induced colitis mice by increasing the proportion of the unidentified_S24_7 and decreasing the relative abundance of unidentified_Ruminococcaceae, Clostridium and Roseburia. On the analysis of SCFAs, the caecal content of acetic acid, propionic acid, isobutyric acid, buturic, and the total SCFAs showed a significant increase in algal oil-administered mice. Together, these results suggested that algal oil rich in DHA inhibited the progress of DSS-induced colitis in mice by modulating the intestinal microbiota and metabolites and repairing the intestinal barrier, which may be applied in the development of therapeutics for intestinal inflammation.
| S-EPMC7772400 | biostudies-literature
Project description:Inflammatory bowel diseases encompass gastrointestinal illnesseses typified by chronic inflammation, loss of epithelial integrity and gastrointestinal microbiota dysbiosis. In an effort to counteract these characteristic perturbations, we used stem cells and/or a probiotic preparation in a murine model of Dextran Sodium Sulfate induced colitis to examine both their efficacy in ameliorating disease and impact on niche-specific microbial communities of the lower GI tract. Colitis was induced in C57BL/6 mice by administering 3% DSS in drinking water for 10 days prior to administering one of three treatment plans: daily probiotic (VSL#3) supplementation for 3 days, a single tail vein injection of 1x106 murine mesenchymal stem cells, or both. Controls included DSS-untreated mice and DSS-treated mice that received no therapy. Ileal, cecal and colonic sections were collected for microbiota and histological analyses. Microbiota profiling revealed distinct bacterial community compositions in the ileum, cecum and colon of control untreated animals, all of which were predicted in silico to be enriched for a number of discrete KEGG pathways, indicating compositional and functional niche specificity in healthy animals. DSS- treatment perturbed community composition in all three niches with ileal communities exhibiting the greatest change relative to control animals. Stem cell, VSL#3 and the combination treated animals exhibited treatment-specific microbiota composition in the lower GI tract, though disease scores were only improved in VSL#3 treated animals. This VSL#3-associated shift in the ileal microbiota was characterized by significant Enterobacteriaceae enrichment compared to colitic animals (p<0.05), Mice (n=40) were randomly divided into five experimental groups, four of which received Dextran Sodium Sulfate (DSS; 3% solution in drinking water) for 10 days to induce colitis. Three of the DSS-treated groups received the following treatment modalities: VSL#3 (VSL#3, n=5), mesenchymal stem cells (MSC, n=5), or VSL#3 + mesenchymal stem cells (DUAL, n=5). The fourth DSS-treated group received no intervention (DSS; n=10). The additional fifth group of animals received neither DSS nor any therapeutic intervention and acted as untreated controls (CNTL, n=15). Following colitis induction (Day 10), DSS administration was halted and mice in the VSL#3, MSC and DUAL groups received the following interventions respectively: daily oral supplementation with 5x106 CFUs per supplement of VSL#3 in 100ul PBS (VSL#3); a single tail vein injection of 1x106 murine mesenchymal stem cells in 100_l PBS on Day 10 (MSC) or a combination of both treatments To provide control data for comparison, CNTL mice (n=5 per time point) were euthanized and sampled on days 1, 10, and 14, while DSS mice (n=5 per time point) were euthanized on days 10 and 14. All MSC, VSL#3, and DUAL mice were euthanized on Day 14. Samples collected from each animal included terminal ileum (1cm proximal to the cecum), cecum (divided transversely and stored as two separate samples), and proximal colon. All samples were added to RNAlater, prior to storage at -80C for analysis. Additional colonic samples were obtained, proximal to the initial sample site for microbiome analyses, and were preserved in paraformaldehyde for histological analyses.
2014-09-01 | E-GEOD-56137 | biostudies-arrayexpress
Project description:Nigella A, also named Sieboldianoside A, has been extracted from many kinds of Traditional Chinese Medicine (TCM), such as Nigella glandulifera, Stauntonia chinensis DC., and the leaves of Acanthopanax sieboldianus. Nigella A exhibited potential analgesic, anti-inflammatory, anti-tumor, and antioxidant activities. However, whether Nigella A could treat ulcerative colitis (UC) is still unknown. As saponins always be regarded as the kinds of ingredients that could regulate immunity and intestinal flora. This research aimed to investigate the therapeutic effect of Nigella A on UC and explore its effect on intestinal flora. We noted that Nigella A and Sulfasalazine (SASP) could significantly improve the signs and symptoms, alleviate colonic pathological injury in DSS-induced mice. The changing of many specific bacterial genus such as Lactobacillus, Porphyromonadaceae, Bacteroides and Escherichia might closely related to the recovery of intestinal inflammatory response. This study initially confirmed the therapeutic effect of Nigella A and SASP on DSS-induced colitis by improving the diversity of intestinal microbial composition. Nigella A has the potential to be developed for the treatment of UC and other disorders related to the imbalance of intestinal flora.
| S-EPMC7533278 | biostudies-literature
Project description:BackgroundThe gut microbiota plays a central role in host physiology and in several pathological mechanisms in humans. Antibiotics compromise the composition and functions of the gut microbiota inducing long-lasting detrimental effects on the host. Recent studies suggest that the efficacy of different clinical therapies depends on the action of the gut microbiota. Here, we investigated how different antibiotic treatments affect the ability of the gut microbiota to control intestinal inflammation upon fecal microbiota transplantation in an experimental colitis model and in ex vivo experiments with human intestinal biopsies.ResultsMurine fecal donors were pre-treated with different antibiotics, i.e., vancomycin, streptomycin, and metronidazole before FMT administration to colitic animals. The analysis of the gut microbiome, fecal metabolome, and the immunophenotyping of colonic lamina propria immune cells revealed that antibiotic pre-treatment significantly influences the capability of the microbiota to control intestinal inflammation. Streptomycin and vancomycin-treated microbiota failed to control intestinal inflammation and were characterized by the blooming of pathobionts previously associated with IBD as well as with metabolites related to the presence of oxidative stress and metabolism of simple sugars. On the contrary, the metronidazole-treated microbiota retained its ability to control inflammation co-occurring with the enrichment of Lactobacillus and of innate immune responses involving iNKT cells. Furthermore, ex vivo cultures of human intestinal lamina propria mononuclear cells and iNKT cell clones from IBD patients with vancomycin pre-treated sterile fecal water showed a Th1/Th17 skewing in CD4+ T-cell populations; metronidazole, on the other hand, induced the polarization of iNKT cells toward the production of IL10.ConclusionsDiverse antibiotic regimens affect the ability of the gut microbiota to control intestinal inflammation in experimental colitis by altering the microbial community structure and microbiota-derived metabolites. Video Abstract.
| S-EPMC7868014 | biostudies-literature