Staphylococcus aureus is a highly successful pathogen that can circumvent many aspects of immunity. Neutrophils, the most abundant of our white blood cells, are a critical defence against infection and yet S. aureus is able to render them ineffective. S. aureus does this by rupturing an intracellular neutrophil compartment known as the phagolysosome, which is where bacteria are normally contained and killed. Escape from the inhospitable phagolysosome allows S. aureus to replicate inside the neutrophil cytosol, eventually bursting the neutrophil open and becoming free to cause infection elsewhere. This project will use super-resolution and confocal microscopy techniques to determine how S. aureus disables the immune response in this way, observing interactions of S. aureus with subcellular components of human neutrophils on a molecular level, visualising early sub-cellular trafficking of the bacteria, interactions with endogenous microbicidal factors, phagosome lysis and escape on a molecular level. The ultimate aim of this project is to identify ways of preventing escape of S. aureus from the phagosome, in order to improve the host defence against this multi-drug resistant and life-threatening microorganism. Publications
Yang D, Ho YX, Cowell LM, Jilani I, Foster SJ and Prince LR. A Genome-Wide Screen Identifies Factors Involved in S. aureus-Induced Human Neutrophil Cell Death and Pathogenesis. Front. Immunol. 2019 10:45. DOI: 10.3389/fimmu.2019.00045 |
The Team
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