School of Medicine
Area of interest
My lab studies inflammasome sensors in the innate immune system. Inflammasomes survey the cytosolic compartment for contamination or perturbation during infection. For example, we have shown that the NLRC4 inflammasome detects bacterial flagellin and type III secretion rod and needle apparatus proteins when they contaminate the cytosol of macrophages. Canonical inflammasomes, such as NLRC4, activate caspase-1, resulting in secretion of IL-1b and IL-18, as well as triggering a form of lytic programmed cell death called pyroptosis. Recently we also began to study the non-canonical inflammasome pathway that activates caspase-11, triggering pyroptosis. Caspase-11 responds to LPS, a component of the Gram-negative membrane, when it contaminates the cytosolic compartment. This protects animals against infection by cytosol invasive bacteria, such as Burkholderia species. However, this pathway is detrimental during overwhelming infection, and causes shock independently from the extracellular LPS sensor, TLR4.
Ongoing studies examine the benefical and detrimental role of pyroptosis, and the canonical and non-canonical inflammasomes in infection and immunopathology.
Awards and Honors
1993 Howard Hughes Summer Honors Advanced Research Program
1997-2000 Poncin Scholarship
2000 Helen Riaboff Whitely Endowed Fellowship Award
2000-2002 Paul Allen Foundation Fellowship Award