Stallings Lab Research


Research in the Stallings Laboratory seeks to better understand the incredible ability of Mycobacterium tuberculosis to withstand hostile conditions during infection and persist for the lifetime of the host.

M. tuberculosis infection begins when inhaled bacilli enter the airways and are immediately exposed to phagocytic cells of the innate immune system. Infection of naive alveolar macrophages and dendritic cells leads to a proinflammatory response and the recruitment of lymphocytes, monocytes, and fibroblasts to form a granuloma. Within the granuloma, the infected cells are activated to kill the intracellular bacteria by imposing an arsenal of stresses. Despite this onslaught of stresses, the bacteria are able to persist for the lifetime of the host, indicating that M. tuberculosis mounts a significant defense against the immune system.

We have identified a number of mycobacterial proteins that function as mediators of mycobacterial stress responses and are required for pathogenesis. Our lab continues to investigate the roles of these proteins during infection and how their activities can be inhibited in new chemotherapeutic strategies to treat mycobacterial infections. In addition, we are investigating the host responses necessary to control M. tuberculosis infection and prevent active tuberculosis disease.