Host-Pathogen Seminar Series 2008-2009

Beth A. McCormick, Ph.D., Professor of Microbiology, Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School

Dr. McCormick's laboratory is interested in molecular mechanisms by which enteric pathogens, namely Salmonella enterica serovar Typhimurium and Shigella flexneri, orchestrate mucosal inflammatory responses.  Such inflammatory responses lead to active states of intestinal inflammation and are a hallmark feature of the disease pathophysiology of inflammatory bowel disease (i.e., Crohn's disease and ulcerative colitis). Research projects in the laboratory are directed at studying host-pathogen interactions that promote gastroenteritis with the goal of developing novel therapeutics for the treatment of inflammatory bowel disease and cancer.

"The ABC's of Salmonella enterica serovar Typhimurium pathogenesis"

David Underhill PhD, Imunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles

A central question in phagocyte biology is to understand how inflammatory responses are tailored to specific microbial infections. As a model for understanding of how different "innate immune receptors" in macrophages and dendritic cells can work together to orchestrate very specific inflammatory responses, the Underhill laboratory has been characterizing the coordinated recognition of fungal pathogens by the C-type lectin receptor Dectin-1, and the Toll-like receptor TLR2. From these studies, we hypothesize that phagosomes are scaffolds for assembly of inflammatory signaling molecules, and that phagocytosis itself is a component of tailoring inflammatory cytokine and chemokine production and polarization of adaptive immune responses. Our laboratory is exploring how innate immune receptors shape adaptive immune responses, and how regulating the behavior of these receptors may be useful for treating inflammatory diseases or in the development of vaccines.
 

Dr. Michael S. Gilmore, Professor of Ophthalmology, Harvard Medical School and President & CEO, Schepens Eye Research Institute 

In addition to being leading causes of antibiotic resistant infection, the enterococci, streptococci and staphylococci are also highly adapted members of the human commensal flora. As a result, these organisms possess sophisticated mechanisms for colonizing human mucosal surfaces and skin, and interaction with the host immune system is finely balanced. Understanding the pathogenesis of infection caused by these bacteria requires an understanding of how host and microbial factors contribute to this fine balance.

"Antibiotic resistant enterococci: What makes a good commensal go bad?"