Project details

The majority of people who get infected with the tuberculosis (TB) bacteria do not get sick. Given there are billions of latently infected individuals globally, the only way to eradicate TB is by stopping people developing disease when infected.

Using lung and blood samples collected from a longitudinal cohort of TB household contacts, this project will investigate how differences in immune cells, the lung microbiome and the inflammatory environment of these tissues differ between people who remain completely uninfected and those who develop disease.

This project will utilise a systems biology approach applying RNAseq, tissue proteomics, cellular phenotyping and microbiome analysis to identify mechanisms of human TB protective immunity and disease risk. 

About our research group

We research how the response of innate immune cells which engulf the tuberculosis (TB) bacteria, namely macrophages, neutrophils and dendritic cells is dysregulated by known TB risk factors. We combine analysis of clinical samples to identify novel pathways of pathogenesis in humans, with in vitro models of TB and HIV infection to identify the molecular mechanism underlying disease risk.  

This includes genetic and epigenetic changes in both the host and bacteria and how these impact the inflammatory response during infection. We are particularly interested in regulation of cell death and the heterogeneity of cellular responses due to tissue micro-environmental changes which we probe using single cell techniques and advanced live cell imaging. We also conduct biomarker discovery for prediction of infection and TB risk.