报告题目1:  Dynamics of the Human Microbiome

报  告 人：Prof. Rob Knight

Departments of Pediatrics and Computer Science & Engineering, University of California at San Diego

报告题目2：Gut microbiota and metabolic diseases: from association to isolation to causation to translation

报  告 人：Prof. Liping Zhao

School of Life Sciences and Biotechnology, Shanghai Jiao Tong University;

Shanghai Center for Systems Biomedicine

肠道菌群高通量测序数据分析的培训演示

培训人：徐振江博士、张晨虹博士、王景

 

时间：2015年9月7日下午13:30-16:30

地点：瑞金二路197号 瑞金医院科教楼2楼报告厅

联系人：张晓君 13761960889, This e-mail address is being protected from spambots. You need JavaScript enabled to view it.

 

Abstract for Rob’s talk:

Advances in technology allow us to understand the human microbiota not as a static entity but as a complex, changing ecosystem that records substantial data about our lifestyles, our environmental exposures, and the people we live with. Here I discuss changes in the human microbiota associated with early life events such as delivery mode and antibiotics, the subsequent development of the microbiome throughout life, and even the development of the microbiome after death and its potential utility for forensics. Of particular value for toxicological studies is the ability to transfer the microbiome to germ-free mice, allowing individualized tests of function and subsequent therapies to be tested in personalized rodent models. Relating human to rodent microbiome timescales, especially for dietary studies, and relating multi-omics data in a timeseries context, remain outstanding challenges. Rapid progress is being made in these areas, and will allow far more powerful studies of the effects of drugs in mammalian hosts and our ability to stratify responders from non-responders for a wide range of therapies.

 

Abstract for Liping’s talk:

Human phenotypes are dictated by the information contents of and molecular crosstalk between the genome and the microbiome. The harmonious integration between human genome and microbiome is the foundation for maintaining a healthy phenome. Poorly balanced diets can turn the gut microbiome from a partner for health to a “pathogen” in chronic diseases. Accumulating evidence supports the new hypothesis that obesity and related metabolic diseases develop because of low-grade, systemic and chronic inflammation induced by endotoxin released into bloodstream from a diet-disrupted gut microbiota. For example, our study showed that an endotoxin-producing bacterium Enterobacter cloacae B29 isolated from the gut of a morbidly obese human volunteer can cause fully developed obesity phenotypes including systemic inflammation, adiposity and insulin resistance when mono-associated with germfree mice. This indicates that specific members of the gut microbiota have the genetic potential to contribute significantly to the development of metabolic disease phenotypes. Thus, the contribution of microbiome to human metabolic phenome must be taken into account when assessing human health. Due to the tight integration of gut microbiota into human global metabolism, molecular profiling of urine metabolites can provide a new window for reflecting physiological functions of gut microbiome. Changes of gut microbiota and urine metabolites can thus be correlated to find out “who des what in the microbiome”.  Using this strategy in our recent study on dietary alleviation of human genetic obesity in Prader-Willi Syndrome, we assembled more than 100 high quality draft genomes of prevalent gut bacteria directly from a large metagenomic dataset. Correlation analysis between abundance of these genomes and urine concentration of metabolites identified specific bacteria, which carry the genes for enzymes required to ferment choline into TMA, a precursor of TMAO, a metabolic toxin for inducing atherosclerosis, indicating that these bacteria may contribute to metabolic deteriorations in the hosts. Understanding the contribution of gut microbiota to human metabolic phenome can lead to new insights on mechanisms of chronic diseases such as obesity and diabetes and development of new measures for their management.