Project description:Interventions: Colorectal cancer control group:no;Colorectal cancer probiotics group:No
Primary outcome(s): Intestinal flora metabolomics;Intestinal mucosal barrier;Inflammatory factors;Observation of clinical efficacy indicators;Intestinal flora
Study Design: Parallel
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. Thus, we hypothesis that asthmatic BSM cell metabolism is modified compare to that of non-asthmatic and that could be a potential target to reduce asthmatic BSM cell proliferation and remodeling in asthma.
Project description:Starting from the evidences of gut microbiota role in tumor development, progression and response to therapy, this project was aimed at evaluating the effect of antibiotic treatment on intestine. The intestinal flora of FVB mice was altered by the oral administration of vancomicyn, mice were then injected with MI6 cells, a singeneic tumor cells line established from spontanueous mammary tumor developped in transgenic d16HER2-transgenic mice [Castagnoli L, 2014]. To analyze the impact of vancomycin on intestinal mucosa, a gene expression profile was performed on colon and ileum samples.
Project description:Antibiotic use is a risk factor for development of inflammatory bowel diseases (IBDs). IBDs are characterized by a damaged mucus layer, which does not properly separate the host intestinal epithelium from the microbiota. Here, we hypothesized that antibiotics might affect the integrity of the mucus barrier. By systematically determining the effects of different antibiotics on mucus layer penetrability we found that oral antibiotic treatment led to breakdown of the mucus barrier and penetration of bacteria into the mucus layer. Using fecal microbiota transplant, RNA sequencing followed by machine learning and ex vivo mucus secretion measurements, we determined that antibiotic treatment induces ER stress and inhibits colonic mucus secretion in a microbiota-independent manner. This mucus secretion flaw led to penetration of bacteria into the colonic mucus layer, translocation of microbial antigens into circulation and exacerbation of ulcerations in a mouse model of IBD. Thus, antibiotic use might predispose to development of intestinal inflammation by impeding mucus production.
Project description:Antibiotic use is a risk factor for development of inflammatory bowel diseases (IBDs). IBDs are characterized by a damaged mucus layer, which does not properly separate the host intestinal epithelium from the microbiota. Here, we hypothesized that antibiotics might affect the integrity of the mucus barrier. By systematically determining the effects of different antibiotics on mucus layer penetrability we found that oral antibiotic treatment led to breakdown of the mucus barrier and penetration of bacteria into the mucus layer. Using fecal microbiota transplant, RNA sequencing followed by machine learning and ex vivo mucus secretion measurements, we determined that antibiotic treatment induces ER stress and inhibits colonic mucus secretion in a microbiota-independent manner. This mucus secretion flaw led to penetration of bacteria into the colonic mucus layer, translocation of microbial antigens into circulation and exacerbation of ulcerations in a mouse model of IBD. Thus, antibiotic use might predispose to development of intestinal inflammation by impeding mucus production.
Project description:Asthma is a very frequent airway disease that affects 6 to 20% of the population. Severe asthma, represents 3 to 5% of all asthmatic patients and is histologically characterized by an increased bronchial smooth muscle (BSM) mass and clinically by viral exacerbations. Functionally, BSM remodeling had a poor prognostic value in asthma, since higher BSM mass was associated with lower lung function and increased exacerbation rate. However, the role of BSM as a potential actor of asthma exacerbation has only been sparsely suggested. We thus hypothesis that asthmatic BSM cells could act on bronchial epithelium and modified its response to rhinovirus infection.
Project description:Next generation sequencing (NGS) results demonstrate the modulative capacity of LCPUFAs on dysregulated miRNA expression in asthma. Methods: Sequencing of miRNA was performed by NGS from lung tissue of asthmatic and control mice with normal diet, as well as of LCPUFA supplemented asthmatic mice using Illumina miSeq. Conclusion: Our results demonstrate the modulative capacity of LCPUFAs on dysregulated miRNA expression in asthma.
Project description:Acute superior mesenteric vein thrombosis (ASMVT) decreases the expression of junction-associated proteins and the number of intestinal epithelial cells, which leads to intestinal epithelial barrier disruption. Thermoprotein deposition has also recently been identified as an important cause of mucosal barrier defects. However, the role and mechanism of thermoprotein deposition in asmvt is not fully understood. Differentially expressed microRNAs (miRNAs) in the intestinal tissues of ASMVT mice were detected by transcriptome sequencing (RNA-Seq). To identify miRNAs involved in intestinal barrier disruption, we performed RNA-Seq analysis of intestinal tissues from ASMVT mice . Sixty miRNAs were abnormally expressed in normal intestinal tissues compared with ASMVT-induced intestinal tissues.