Macrophages and neutrophils deploy a variety of antimicrobial mechanisms to recruit additional immune cells and directly kill pathogens. However, Y. pestis actively inhibits these important responses to evade phagocytic killing and to slow inflammation needed to control bacterial spread.

Our lab is working to define:

1) the role of inflammatory lipids during plague

2) the impact of manipulation of host extracellular vesicles by Y. pestis on inflammation

3) the specific mechanisms used by Y. pestis to evade killing by macrophages

Zinc is required for growth of Y. pestis (and other bacteria). As such, eukaryotic organisms have developed mechanisms that limit zinc availability, restricting growth of invading bacteria. However, Y. pestis has evolved high-affinity metal acquisition systems.

Our lab is working to understand:

1) how these metal acquisition systems work

2) how zinc acquisition contributes to Y. pestis pathogenesis

3) the potential for metal acquisition systems to serve as therapeutic targets

Multidrug resistant (MDR) bacteria have developed resistance to most — and in some cases all — of the antimicrobials currently available in the clinic. Without the development of new drugs, even simple, routine procedures run the risk of introducing life-threating infections to patients.

Our lab is working to develop preclinical models that help identify and test new antimicrobials against MDR bacteria.