David Schneider
Academic Appointments
- Associate Professor, Microbiology & Immunology
Contact Information
- Academic
Offices
Personal Information Email Tel (650) 724-8064
Professional Snapshot
Postdoctoral Advisees
Graduate & Fellowship Program Affiliations
Web Site Links
Scientific Focus
Research Interests
We study innate immunity and microbial pathogenesis. We have been studying models for a variety of bacterial infections including: Listeria, Mycobacteria, Salmonella and Streptococcus as well as some fungi, parasites and viruses..
We work at both cellular and whole animal levels. Work at cellular level helps us discover what a microorganism must do survive in a hostile environment like a macrophage. Studies at the whole organism level let us understand the larger physiological processes that decide whether we live or die.
All of our projects start with the fruit fly Drosophila melanogaster and we use the fly in two ways: first, as a model human, to study how bacterial pathogens like Mycobacterium, Listeria and Salmonella survive within phagocytes, second, as a model mosquito, to determine how insects act as vectors for diseases like malaria.
The reason for starting with Drosophila is its vast array of tools. Our principal tool is genetics and we use genetic manipulations of both the fly and pathogens to probe host-pathogen interactions. Genetic transformation, transcriptome analysis and in vitro studies using cultured phagocytes complement our genetic screens.
Publications
- The role of anorexia in resistance and tolerance to infections in Drosophila. PLoS Biol. 2009; (7): e1000150
- Relating immune and stress responses to infection resistance and tolerance. Brain Behav Immun. 2009
- The Imd pathway is involved in antiviral immune responses in Drosophila. PLoS One. 2009; (10): e7436
- Pathogenesis of listeria-infected Drosophila wntD mutants is associated with elevated levels of the novel immunity gene edin. PLoS Pathog. 2008; (7): e1000111
- Identification of Drosophila mutants altering defense of and endurance to Listeria monocytogenes infection. Genetics. 2008; (3): 1807-15

