Biotechnology and Bioengineering Department
(925) 294-6751 / email@example.com
My primary scientific interest is in microbial development and its implications for human disease. Currently my research is focused on two different aspects of host–pathogen interactions: (1) spore germination, a developmental process central to anthrax pathogenesis, and (2) the host’s innate immune response to bacterial pathogens.
Germination studies. Germination is the developmental process by which microbial spores break dormancy and return to active growth. Despite the importance of germination to the life cycle of many a microbe, our understanding of this process is surprisingly rudimentary. We have initiated a comprehensive analysis of the molecular, biochemical, and biophysical events that together constitute germination in Bacillus anthracis, the causitive agent of anthrax disease. Innovative new technologies developed at Sandia should enable us to overcome many of the technical challenges that have confounded previous studies of germination. Knowledge gained through this research should not only provide new insight into a fundamental cellular process but also inform ongoing efforts to develop new anti-anthrax countermeasures, including prophylactics, therapeutics, detoxification strategies, and detection systems.
Macrophase response to bacterial pathogens. The innate immune system represents the host’s first line of defense against microbial pathogens. Sentry cells such as macrophages detect pathogen-associated molecular patterns using toll-like receptors (TLRs). The activation of a TLR sets in motion a signal transduction cascade; signals from different TLRs converge and ultimately determine the macrophage’s initial response to the pathogen. As part of a large consortium of Sandia labs, and in collaboration with partners at the University of Texas Medical Branch and the University of California, San Francisco, we are using novel microfluidics, imaging, and computational technologies to analyze macrophage response to the bacterial pathogens Francisella tularensis and Yersinia pestis. This work should lead to a more precise and comprehensive understanding of the TLR signaling network and the means by which pathogens subvert it.