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Microbiota-immune interactions that promote intestinal homeostasis

促进肠道稳态的微生物群-免疫相互作用

基本信息

批准号：
10626869
负责人：
June Louise Round
金额：
$ 60.61万
依托单位：
UNIVERSITY OF UTAH
依托单位国家：
美国
项目类别：
财政年份：
2021
资助国家：
美国
起止时间：
2021-06-15 至 2026-05-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10626869
关键词：
Adipose tissue Age Animals Bacteria Binding CD36 Antigens CD36 gene Ceramides Chronic Colitis Collection Communities Complex Crohn&apos s disease Data Defect Desulfovibrio Development Diabetes Mellitus Disease Disease Progression Disease model Germ-Free Gnotobiotic Human Immune Immune system Immunity Immunoglobulin A Incidence Individual Inflammation Inflammatory Inflammatory Bowel Diseases Insulin Resistance Intestinal permeability Intestines Investigation Link Lipids Maintenance Metabolic Metabolic Diseases Metabolic syndrome Metabolism Metagenomics Microbe Obesity Oral Organism Pathway interactions Patients Population Prevention Production Publishing Relapse Role Sampling Series Systems Development Testing Therapeutic Therapeutic Intervention Therapeutic Uses Ulcerative Colitis Weight Gain absorption commensal bacteria experimental study gut health gut homeostasis gut inflammation gut microbes intestinal homeostasis member microbial microbial composition microbial products microbiota microbiota transplantation microorganism interaction mouse model novel novel marker prevent response sulfate reducing bacteria therapeutic development

项目摘要

ABSTRACT Individuals with inflammatory bowel disease (IBD) are more likely to develop metabolic abnormalities, such as diabetes, however little is known about the basis of this connection. Multiple studies have now shown that changes to the composition of the microbiota are a factor in multiple diseases, including IBD and diabetes. Moreover, the studies that have examined the composition of the microbiota within individuals with IBD or diabetes, have identified similar changes to these resident communities. We have recently identified a mouse model that develops worsened colitis and spontaneous obesity and insulin resistance. Both of these diseases are reliant on the microbiota and can be rescued by a microbiota transplant, or an oral gavage of a purified population of Clostridia. Thus, we hypothesize that the growing incidence of IBD and diabetes may be attributable to similar defects in the microbiota and might explain the why some individuals are more prone to develop both diseases. Based on this, we propose a series of experiments to identify a defined consortia of Clostridia that will function to prevent disease and explore the common mechanisms, including effects of the immune system, between IBD and metabolism that might lead to the development of these diseases. Thus, our findings will be among the first to identify a consortia of bacteria that could be used for therapeutic intervention/prevention of IBD and/or diabetes and allow for an in-depth mechanistic understanding of how these protective bacteria maintain intestinal homeostasis.

摘要