Amanda Jamieson

Assistant Professor of Molecular Microbiology and Immunology
Brown University
171 Meeting Street
Providence RI 02912
1 (401) 863-6158

Amanda M. Jamieson, PhD


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. In 2014 Dr. Jamieson received the Salomon Research Award and the Brazil Initiative Collaboration Grant. She is an author on 30 peer-reviewed publications, and has been invited to speak both nationally and internationally. 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.

COBRE Abstract

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.

Project Updates