Denise M. Monack
Academic Appointments
- Associate Professor, Microbiology & Immunology
- Member, Child Health Research Institute
Key Documents
Contact Information
- Academic Offices
Alternate Contact Sara Fisher Email
Professional Overview
Honors and Awards
- Burroughs Wellcome Fund Recipient in Infectious Disease, The Burroughs Wellcome Fund (11/01/09-10/31/15)
- G.J. Thorbecke Award, Society of Leukocyte Biology (2010)
- Sidney Raffel Award for Outstanding Accomplishment in Graduate Study, Stanford University (2001)
- Baxter Faculty Scholar Award, Baxter Foundation (May 2008)
- Terman Fellowship, Terman Fellows Program (10/1/08-9/30/11)
Graduate & Fellowship Program Affiliations
Scientific Focus
Current Research Interests
The primary focus of my research is to understand the genetic and molecular mechanisms of intracellular bacterial pathogenesis. We use two model systems, Salmonella typhimurium and Francisella tularensis, to study the complex host-pathogen interactions.
Both of these organisms survive and multiply in macrophages, an important immune effector cell. Macrophages express Pattern Recognition Receptors on the surface as well as in the cytosol. My laboratory focuses on the cytosolic recognition of bacteria that leads to Type I Interferon signaling and Inflammasome activation. We take both a genetic and biochemical approach to understand the molecular mechanisms involved in host recognition pathways leading to inflammation and pathogen evasion mechanisms.
Salmonella typhi causes the systemic disease typhoid fever and Francisella tularensis causes the systemic disease tularemia (rabbit fever). Utilizing mouse models of systemic salmonellosis and tularemia, we would like to understand how Salmonella persists within certain hosts for years in the face of a robust immune response and how F. tularensis, a stealth invader, can cause a rapid, lethal infection.
Publications
- Policing the cytosol--bacterial-sensing inflammasome receptors and pathways. Curr Opin Immunol. 2013; (1): 34-9
- The NeST long ncRNA controls microbial susceptibility and epigenetic activation of the interferon-γ locus. Cell. 2013; (4): 743-54
- Innate immune response to Salmonella typhimurium, a model enteric pathogen. Gut Microbes. 2012 Mar-Apr; (2): 62-70
- Caspase-1 activity is required to bypass macrophage apoptosis upon Salmonella infection. Nat Chem Biol. 2012; (9): 745-7
- Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1. Nature. 2012; (7419): 288-91
- Delayed activation of host innate immune pathways in streptozotocin-induced diabetic hosts leads to more severe disease during infection with Burkholderia pseudomallei. Immunology. 2012; (4): 312-32
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