Suchergebnisse

Relación dieta-microbioma; Validación relativa; Desarrollo de sFFQ ; Relació dieta-microbioma; Validació relativa; Desenvolupament sFFQ ; Diet–microbiome relationship; Relative validation; sFFQ development ; Diet is recognised as the main driver of changes in gut microbiota. However, linking habitual dietary intake to microbiome composition and activity remains a challenge, leaving most microbiome studies with little or no dietary information. To fill this knowledge gap, we conducted two consecutive studies (n = 84: a first pilot study (n = 40) to build a web-based, semi-quantitative simplified FFQ (sFFQ) based on three 24-h dietary recalls (24HRs); a second study (n = 44) served to validate the newly developed sFFQ using three 24HRs as reference method and to relate gut microbiome profiling (16S rRNA gene) with the extracted dietary and lifestyle data. Relative validation analysis provided acceptable classification and agreement for 13 out of 24 (54%) food groups and 20 out of 29 nutrients (69%) based on intraclass correlation coefficient, cross-classification, Spearman's correlation, Wilcoxon test, and Bland–Altman. Microbiome analysis showed that higher diversity was positively associated with age, vaginal birth, and intake of fruit. In contrast, microbial diversity was negatively associated with BMI, processed meats, ready-to-eat meals, sodium, and saturated fat. Our analysis also revealed a correlation between food groups or nutrients and microbial composition. Overall, we provide the first dietary assessment tool to be validated and correlated with microbiome data for population studies. ; This study was supported by grants from by the Instituto de Salud Carlos III/FEDER (PI17/00614; PI20/00130), a government agency. Francisca Yáñez was supported by a fellowship from ANID, BECAS Chile, No. 72190278. Zixuan Xie received a fellowship from the European Union's Horizon 2020 research and innovation program under the Marie Sklodowska-Curie Action, Innovative Training Network: FunHoMic; grant number 812969.

Inflammatory bowel disease; Faecal microbiota transplantation; Rat model of colitis ; Enfermedad inflamatoria intestinal; Trasplante de microbiota fecal; Modelo de colitis en ratas ; Malaltia inflamatòria intestinal; Trasplantament de microbiota fecal; Model de colitis en rates ; Background: Faecal microbiota transplantation (FMT) is a novel potential therapy for inflammatory bowel diseases, but it is poorly characterised. Methods: We evaluated the performance of the mouse and rat as a pre-clinical model for human microbiota engraftment. We then characterised the effect of a single human stool transfer (HST) on a humanised model of DSS-induced colitis. Colonic and faecal microbial communities were analysed using the 16S rRNA approach and clinical manifestations were assessed in a longitudinal setting. Findings: The microbial community of rats showed greater similarity to that of humans, while the microbiome of mice showed less similarity to that of humans. Moreover, rats captured more human microbial species than mice after a single HST. Using the rat model, we showed that HST compensated faecal dysbiosis by restoring alpha-diversity and by increasing the relative abundance of health-related microbial genera. To some extent, HST also modulated the microbial composition of colonic tissue. These faecal and colonic microbial communities alterations led to a relative restoration of colon length, and a significant decrease in both epithelium damage and disease severity. Remarkably, stopping inflammation by removing DSS before HST caused a faster and greater recovery of both microbiome and clinical manifestation features. Interpretation: Our results indicate that the rat outperforms the mouse as a model for human microbiota engraftment and show that the efficacy of HST can be enhanced when inflammation stimulation is withdrawn. Finally, our findings support a new therapeutic strategy based on the use FMT combined with anti inflammatory drugs. ; Study funded by the Instituto de Salud Carlos III/FEDER (PI17/00614), a government agency. The funder had no role in study design, data collection, data analysis, interpretation or writing of the report.

Citocines; Malalties del fetge ; Citocinas, Enfermedades del hígado ; Cytokines; Liver diseases ; Probiotics can prevent pathological bacterial translocation by modulating intestinal microbiota and improving the gut barrier. The aim was to evaluate the effect of a fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I-1518 on bacterial translocation in rats with carbon tetrachloride (CCl4)-induced cirrhosis. Sprague-Dawley rats treated with CCl4 were randomized into a probiotic group that received fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I-1518 in drinking water or a water group that received water only. Laparotomy was performed one week after ascites development. We evaluated bacterial translocation, intestinal microbiota, the intestinal barrier and cytokines in mesenteric lymph nodes and serum. Bacterial translocation decreased and gut dysbiosis improved in the probiotic group compared to the water group. The ileal β-defensin-1 concentration was higher and ileal malondialdehyde levels were lower in the probiotic group than in water group. There were no differences between groups in serum cytokines but TNF-α levels in mesenteric lymph nodes were lower in the probiotic group than in the water group. Fermented milk containing Lactobacillus paracasei subsp. paracasei CNCM I-1518 decreases bacterial translocation, gut dysbiosis and ileal oxidative damage and increases ileal β-defensin-1 expression in rats treated with CCl4, suggesting an improvement in the intestinal barrier integrity. ; This study was partially funded by Danone Research (Palaiseau, Cedex, France), and grants PI08/0262 and PI14/00680 from the Instituto de Salud Carlos III, Madrid, Spain, and cofinanced by Fondos FEDER (Fondo Europeo de Desarrollo Regional), "Una manera de hacer Europa", European Union, and CERCA Programme, Generalitat de Catalunya. The investigational product was provided by Danone Research. Silvia Vidal was supported by Fondo de Investigaciones Sanitarias (FIS) and is a participant in the Program for Stabilization of Investigators of the Direcció d'Estrategia i Coordinació del Departament de Salut, Generalitat de Catalunya. Pau Sancho-Bru is funded by Instituto de Salud Carlos III, Miguel Servet (CP11/00071).

© 2021 The Author(s). ; Crohn's disease (CD) and ulcerative colitis (UC), the two main forms of inflammatory bowel disease (IBD), affect several million people worldwide. CD and UC are characterized by periods of clinical remission and relapse. Although IBD patients present chronic alterations of the gut microbiome, called dysbiosis, little attention has been devoted to the relapse-related microbiome. To address this gap, we generated shotgun metagenomic data from the stools of two European cohorts—134 Spanish (followed up for one year) and 49 Belgian (followed up for 6 months) subjects—to characterize the microbial taxonomic and metabolic profiles present. To assess the predictive value of microbiome data, we added the taxonomic profiles generated from a previous study of 130 Americans. Our results revealed that CD was more dysbiotic than UC compared to healthy controls (HC) and that strategies for energy extraction and propionate production were different in CD compared to UC and HC. Remarkably, CD and UC relapses were not associated with alpha- or beta-diversity, or with a dysbiotic score. However, CD relapse was linked to alterations at the species and metabolic pathway levels, including those involved in propionate production. The random forest method using taxonomic profiles allowed the prediction of CD vs. non-CD with an AUC = 0.938, UC vs. HC with an AUC = 0.646, and CD relapse vs. remission with an AUC = 0.769. Our study validates previous taxonomic findings, points to different relapse-related growth and defence mechanisms in CD compared to UC and HC and provides biomarkers to discriminate IBD subtypes and predict disease activity. ; This study was supported by the Instituto de Salud Carlos III /FEDER, a government agency (grant numbers: PI17/00614; PI20/00130), and by the Crohn's & Colitis Foundation of America (Award ID: 514634).