Amanda M. Jamieson is currently an Assistant Professor of Molecular Microbiology and Immunology at Brown University. She is the Principal Investigator on a 12 month pilot project with the CPVB COBRE entitled: “Impact if Influenza virus/L. pneumophila coinfection on lung endothelial cells”
Dr. Jamieson graduated summa cum laude from Carleton College, and received her Ph.D. from University of California at Berkeley. Her graduate work in Dr. David Raulet’s laboratory focused on the development and activation of cells of the early or innate immune system called Natural Killer (NK) cells. She began her post-doctoral training in the laboratory of Dr. Ruslan Medzhitov at Yale University School of Medicine where she focused on the consequences of viral bacterial coinfections. She continued this work at the University of Vienna, Vienna, Austria as a University Assistant in the laboratory of Dr. Thomas Decker. While at the University of Vienna she served as an instructor for Immunology lecture and laboratory courses, mentored the theses of 3 master’s students, and received two research grants (one as a PI and one as a co-PI) from the Austrian Research Foundation (FWF).
She started her position at Brown University on July 1,2013. Her research focuses on the role of the innate immune system in resistance and resilience responses to complex diseases of the pulmonary and circulatory systems. She is an author on more than 30 peer-reviewed publications, one book chapter, and has been invited to speak both nationally and internationally. Her research is currently funded by Defense Advanced Research Project Agency Young Faculty Award (DARPA) Director’s Award YFA15D15AP00100, NIH/NIGMS COBRE Center for Computational Biology of Human Disease IDeA grant P20GM109035, and NIH/NHLBI 1R01HLI12688701A1
The purpose of this research proposal is to use our mouse model of viral/bacterial lung coinfection to determine the impact that polymicrobial infections have on the lung endothelium. We propose that the ability to survive an infection is determined by two main factors, resistance and tolerance. Resistance is defined as the ability to respond to and clear the pathogen, while tolerance is the ability to withstand the effects of the pathogens and the potentially damaging effects of the immune response. We have developed a mouse model of influenza virus/L. pneumophila coinfection that allows us to study tolerance mechanisms in lung coinfections. In this system there is increased lung damage in coinfected animals without an increase in pathogen burden. The lung endothelium plays important roles in the immune response, and an intact endothelium is necessary for proper lung function. Therefore, the delicate balance between clearing an infection and not causing excessive tissue damage is very apparent in the pulmonary system. We will examine how coinfection alters the immune response, the tolerance response, and the infectivity of pulmonary endothelial cells. Understanding how polymicrobial infections of the lung affect the lung endothelium is crucial to advancing our knowledge of the pulmonary immune response to infectious disease.
Alfred Ayala, PhD, MS
Defense Advanced Research Projects Agency (DARPA) YFAA15
Project Title: Influence of pulmonary infections on the wound healing response.
Funding Source: DARPA
COBRE Center for Computational Biology of Human Disease
Project Title: “Project 3: Tolerance of Viral/Bacterial Co-Infections”
Funding Source: National Institute of Health (NIH) National Institute of General Medical Sciences (NIGMS)
Project Title: Influence of the lung microbiome on macrophage responses to lung damage
Funding Source: NIH/NHLBI
Ocean State Research Institute
Providence VA Medical Center
830 Chalkstone Avenue
Providence RI 02908
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Research reported in this website was supported by the National Institute of General Medical Science of the National Institutes of Health under grant number P20GM103652.