Bryson Lab

Mycobacterium tuberculosis remains one of the world’s most deadly bacteria resulting in infection in nearly a third of the global population and millions of deaths per year. Clinically, tuberculosis is highly variable. Even within one patient, sites of infection can have different outcomes. One of the critical players during infection is the macrophage, an innate immune cell that is among the first to encounter M. tuberculosis. We take the viewpoint of both the bacterium and the macrophage to understand what factors drive the outcome of infection using new technologies and classical approaches. The ultimate goal is to manipulate these cells therapeutically to fight tuberculosis infection.

Recent advances in our understanding of tuberculosis infection demonstrate that infection within a given individual is highly heterogeneous; however, the determinants that drive lesions towards complete bacterial sterilization remain poorly understood. We are interested in developing new tools to dissect the complex dynamics of bacterial infection at a variety of scales ranging from single cells to infected hosts sitting in both “reference frames” by taking both an immunologist’s and a microbiologist’s perspective. Combining new technologies with classical approaches, we are focused ultimately on the goal to manipulate the immune system to improve bacterial control.