The broad goal of this project is to contribute for a better understanding of the molecular mechanisms that contribute for rickettsial pathogenesis. Therefore, we aim at (i) evaluate macrophage permissiveness to infection by rickettsial species responsible for mild rickettsioses, (ii) to define (and compare) the extent of host cell modulation by these rickettsial species in two different cell lines with the utmost relevance for in vivo infections (macrophages and endothelial cells), and (iii) to decipher the role of cellular cross-talk for the development of rickettsial pathogenesis. Combined with previous data, we expect that this project will generate a wealth of information on the host cellular pathways manipulated by rickettsial species to establish a successful infection, which will be instrumental for the development of novel targeted approaches in rickettsioses. Furthermore, by combining the knowledge on the ability to survive and proliferate in macrophages with the host manipulation capacity of Rickettsia species with different degrees of pathogenicity for humans, we aim to develop a prediction model of pathogenicity for rickettsial species.
The goal of the study is to understand the extent of host cell modulation by rickettsial species responsible for mild rickettsioses and to decipher the role of cellular cross-talk in rickettsial pathogenesis.
ESCMID Research Grant 2020