Extracellular vesicles (EVs) are membrane-bound nanovesicles released by virtually all cell types across kingdoms and transport various biomolecules such as proteins, nucleic acids and lipids between cells. EVs play important roles in infectious diseases and have been shown to play important roles in mediating immune activation as well as immune evasion by bacterial-derived EVs. In this project, we aim to isolate and investigate the structure, protein composition and pathological function of EVs produced by human immune cells upon infection by the respiratory tract bacterial pathogen, Streptococcus pneumoniae and its pore-forming toxin, pneumolysin (PLY). We use in-vitro cell culture models, primary cells as well as mouse models to study the role of EVs shed during infection.

We recently discovered that pneumococcal bacteria can also survive intracellularly within dendritic cells and lung alveolar macrophages pneumococci by avoiding fusion with the bactericidal lysosomes and remain viable with the macrophages. In this manner, the macrophages serve as a "silent" persistent reservoir for the bacteria to reestablish colonization and thereby transmit itself to new hosts. Our lab is interested to study the mechanisms that promote bacterial survival within host cells and immunophenotype macrophages that are permissive to bacterial survival.