University of Michigan Medical School, USA
Title: How a host organism responds to various microbial infections and vaccinations?
I am Oliver, Associate Professor in Unit for Laboratory Animal Medicine (ULAM) and Department of Microbiology and Immunology. I am also an affiliated member of the Center for Computational Medicine and Biology (CCMB) and a member of the (Comprehensive Cancer Center) in the University of Michigan (UM) Medical School. Our laboratory research is focused on host-Brucella interaction and bioinformatics. I had my D.V.M. education at Jiangxi Agricultural University and my M.S. degree (Co-advisors: Professors Zhongzhi Zhang and Hanchun Yang) in Infectious Diseases and Veterinary Preventive Medicine at China Agricultural University in China. I obtained my professional assistant veterinarian license during my two-year employment at Beijing Xijiao Livestock and Poultry Company, Beijing, China. My training in Brucella research started in 1996 in Dr. Gerhardt Schurig’s immunology laboratory at the Virginia Polytechnic Institute and State University (Virginia Tech). I obtained my Ph.D. in Dr. Schurig's lab in 2000. I then worked in the same lab as a postdoc for half a year. I obtained my M.S. degree (research advisor: Dr. Pedro Mendes) in computer science in Virginia Tech with a focus on bioinformatics in May 2002. After graduation I worked as a senior research associate for three years in Dr. Bruno Sobral’s group at the Virginia Bioinformatics Institute (VBI). I joined UM in July 2005 as an assistant professor and became an associate professor in September 2011 (with tenure).
With the ever-increasing volume of publications in host-pathogen interactions, it is very challenging to integrate and analyze published big data and knowledge. Our studies have first identified a caspase-2-mediated proinflammatory cell death, which exists in macrophages and dendritic cells infected with a live attenuated vaccineBrucella strainRB51. This type of cell death is different from non-proinflammatory apoptosis or caspase-1-mediatedproinflammatorypyroptosis, and so we named the cell death "caspase-2-mediated pyroptosis". Interestingly, virulent Brucella inhibits such cell death in infected macrophages but not in dendritic cells. Our current confusions are how to understand more about the pathway and how to integrate this pathway with other cell death pathways modulated by variousinfections and vaccinations. To support knowledge integration and advanced data analysis, the presenter proposes an integrative One Network ('OneNet') Theory of Life, which treats the whole process of a life of an organism as a single integrative, complex, and dynamic network (called “OneNet”). Based on this theory, one host organism will utilize a single complex interaction network to respond to different pathogen infections or vaccinations. The OneNet interaction networks of one organism can be better represented and studied using biological ontologies. An ontology is a human- and computer-interpretable set of terms and relations that represent entities in a specific domain and how these terms relate to each other. Like the Periodic Table of Chemical Elements that represents the information of various chemical elements, ontologies can be used to systematically represent and analyze host responses to infections and vaccinations.