In the Stallings Lab, we investigate the contributions of both the host and the pathogen to the outcomes of M. tuberculosis infection.
The Stallings Laboratory (http://stallingslab.wustl.edu/) is currently recruiting postdoctoral researchers to study the molecular details of Mycobacterium tuberculosis pathogenesis. In the Stallings Lab, we investigate the contributions of both the host and the pathogen to the
outcomes of M. tuberculosis infection. We use a combination of microbiology, immunology, molecular biology, biochemistry, cell biology, and animal models of disease to seek better understanding of how M. tuberculosis defends itself against host immune attacks and antibiotic
therapy as well as what immune responses are required to control M. tuberculosis infection. We are recruiting for multiple positions to address the following open questions:
- What innate immune responses are required to control M. tuberculosis infection? Both the disease outcome and the pathology of tuberculosis are driven by the immune response mounted
in the host. Because of the pivotal role of the immune response in tuberculosis, there is interest in developing immunotherapies to control the infection. However, it will be important to understand
what immune responses are required to control M. tuberculosis infection in order to know what pathways to target with these therapies. The Stallings Lab uses a mouse model of infection to
identify and study host proteins required to control M. tuberculosis infection. Future studies will include dissecting the mechanism by which recently identified factors control M. tuberculosis
infection as well as discovering new pathways required for host defense.
- How do neutrophils contribute to the outcome of M. tuberculosis infection? The interactions between neutrophils and M. tuberculosis are the predominant host cell-pathogen interaction during active tuberculosis disease. Nevertheless, in comparison to other immune cells, we know relatively little about the responses of neutrophils to M. tuberculosis infection and how this contributes to disease. Future studies will involve mechanistically dissecting the response of neutrophils to M. tuberculosis infection and determining the impact of modifying these responses on disease progression.
- How does M. tuberculosis defend itself against host immunity and antibiotic therapy to persist during infection? During infection, M. tuberculosis responds to host-derived stresses by changing its physiology to become stress and antibiotic-tolerant. To dissect the mechanisms used by M. tuberculosis to defend itself against the host, the Stallings Lab has recently taken a chemical genetic approach and identified compounds that block M. tuberculosis stress and antibiotic tolerance. Future studies involve investigating the mechanisms by which these compounds block M. tuberculosis tolerance to elucidate previously unknown pathways involved in persistence.
Interested applicants should send their CV, a statement of research interests, and the contact information for three references to Dr. Christina Stallings at [email protected].
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