Infectious Diseases at Brown University with a Focus on the Use of Invertebrate Model Hosts

Title：Prof. Eleftherios Mylonakis
Presenter：Alpert Medical School and Brown University, USA
Time：2013年3月29日16:00-18:00
Vennue：微生物所A102会议室
Chair：黄广华 研究员
Abstract：His work focuses on the study of bacterial and fungal pathogenesis and resistance. His studies have developed a novel alternative to study microbial infection and host response: the use of invertebrate model hosts. These surrogate invertebrate hosts fill an important niche in pathogenesis research and provide a unique opportunity to identify novel antimicrobial compounds and study basic, evolutionarily conserved aspects of virulence and host response. As part of these efforts the Mylonakis group has demonstrated that: 1. There are extensive similarities between infections in mammals and non-vertebrate models including nematode and insect hosts. 2. The model microscopic nematode C. elegans grown on non-pathogenic yeasts has a life span similar to or longer than nematodes fed on the usual laboratory food source, but human pathogens kill C. elegans. 3. A number of virulence traits that are involved in mammalian infection from a variety of pathogens are associated with C. elegans disease. 4. C. elegans assays can be used to identify novel virulence factors that are associated with mammalian infection and these virulence factors provide important insights in microbial biology. 5. Alternative hosts can be used to identify and study compounds with antimicrobial efficacy and multidrug resistance (MDR) mechanisms. 6. During polymicrobial infection, prokaryote-eukaryote interactions modulate virulence. 7. There are evolutionarily conserved pathways for the innate sensing of fungal pathogens. 8. Identified receptors that mediate host defense.

 In summary, these investigations have identified novel virulence factors, cross kingdom pathogen-pathogen interactions, novel antimicrobial agents and evolutionarily conserved traits that are involved in host virulence and immune responses during infection. Taken in their totality, these results indicate that a common, fundamental set of molecular mechanisms is employed by microbial pathogens against a widely divergent array of metazoan hosts.