Rolla E. Dyer Lecture
Established in 1950 in honor of former NIH director Dr. Rolla E. Dyer, a noted authority on infectious diseases. The lectureship, part of the Wednesday Afternoon Lecture Series, features internationally renowned researchers who have contributed substantially to medical as well as biological knowledge of infectious diseases.
Dr. Bumpus’ laboratory uses mass spectrometry and molecular pharmacology based approaches to investigate the biotransformation of clinically used drugs by the cytochromes P450s. The cytochromes P450 are responsible for the metabolism of an estimated 75 percent of currently marketed drugs. Cytochrome P450-mediated biotransformation of drugs most often results in the production of hydrophilic metabolites that can be readily excreted from the body; however, in certain instances toxic metabolites are formed that can stimulate cell death and organ failure.
Increasing prevalence and severity of multi-drug-resistant bacterial infections require novel management strategies. One possible strategy is a renewed approach to ‘phage therapy,’ where these administered viruses not only kill the target bacteria, but also predictably select for phage resistance that reduces virulence and/or increases antibiotic sensitivity (evolutionary trade-offs).
Dr. Cooper’s research program examines the effectiveness of multilevel strategies for advancing health equity in the United States and Sub Saharan Africa. She has conducted observational studies to describe attitudinal barriers to equitable health status and health care among patients from diverse racial and ethnic groups, and to elucidate mechanisms, such as the quality of social relationships, for racial and socioeconomic disparities in health status and healthcare.
Research in the Ghedin Lab meets at the interface of microbiology, genomics, and systems biology. Projects touch on the extent of intra- and inter-host microparasite (viruses and bacteria) diversity within the context of transmission and virulence, and parse the relationship between microbial ecology in the respiratory tract and disease progression.
The Fitzgerald lab is focused on understanding the molecular mechanisms controlling the inflammatory response. We are interested in determining how the immune system discriminates between pathogens, resident microflora and host molecules to both protect the host from infection and avoid damaging inflammatory diseases. We employ multifaceted approaches including immunology, biochemistry, molecular biology and genetics to understand these mechanisms.
Dr. Belkaid work explores the field of immune regulation and has defined fundamental mechanisms that regulate tissue homeostasis and host immune responses. Her work uncovered key roles for the commensal microbiota and dietary factors in the maintenance of tissue immunity and protection to pathogens.
Current research interests are focused on characterization of the structure and function of the microbial communities that are found in the human environment, as part of the NIH-funded Human Microbiome Project, including projects specifically focused on obesity, metabolic syndrome, inflammatory bowel disease, the interactions between the human immune response and the gut microbiome, and the impact of probiotics on the structure and function of the intestinal microbiome.
The Virgin lab issues at the interface between virology and immunology, working from the hypothesis that viruses manipulate the immune response using immunoevasive gene products as the immune response attempts to eradicate the virus. Please see the informative and amusing animated video at http://pathology.wustl.edu/labs/virgin.
Research over the past two decades has led to the fundamental understanding that initiation of immune responses to infectious microorganisms relies on pathogen recognition by innate microbial sensors, collectively known as pattern recognition receptors (PRRs). PRRs fall into several families, each of which recognizes distinct pathogen-associated molecular patterns (PAMPs). Stimulating PRRs results in transcriptional activation of genes involved in innate defense as well as those that activate antigen-presenting cells for successful priming of “adaptive” T- and B-cell responses.
The page was last updated on Thursday, January 29, 2015 - 2:25pm