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

NOTE: This seminar will take place in 170 DHLRI.

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"

Dennis Metzger, Professor and Director, Center for Immunology and Microbial Disease, Albany Medical College

NOTE: This seminar is co-sponsored by the Department of Veterinary Biosciences

Increased susceptibility to secondary bacterial infections often occurs during recovery from viral infection and is a recognized clinical problem that ultimately causes many, if not the majority of deaths during human influenza pandemics, including the 1918 pandemic.  We have now found that the enhanced susceptibility to bacterial infection is mediated by IFN-y produced during the induction of pulmonary T cell responses to influenza virus, which results in inhibition of innate immune defense mechanisms.  Importantly, anti-IFN-y treatment can reverse this effect and thus may provide a new therapeutic approach for protecting the human population from secondary bacterial infections during influenza pandemics.

"Cytokine Regulation of Pulmonary Immunity"

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

NOTE: This seminar is co-sponsored by the Department of Molecular Virology, Immunology and Medical Genetics.

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.

"Phagocytosis and Inflammation - What is the connection?"

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

NOTE: This seminar will start at 4:30pm.

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?"

Thomas J. Braciale, Director, Beirne Carter Center for Immunology Research and Professor of Pathology and Microbiology, University of Virginia

NOTE: This seminar is co-sponsored by the Center for Vaccines and Immunity, Nationwide Children’s Research Institute

Influenza virus is a major human pathogen.  Infection with this virus can cause severe lung Inflammation resulting in significant morbidity and occasional mortality.  The host immune response influenza infection in the respiratory tract is a major contributor to lung injury and the pathology of infection.  We will describe recent work dealing with the control of pulmonary inflammation during experimental influenza infection and the contribution of Interleukin 10 to this process.

"IL-10 and Pulmonary Injury during Influenza Infection: CD8+ T cells control themselves "