We welcome inquiries for rotation projects as well as potential postdoctoral applications. Scroll through our list of active projects to see if you want to get involved in research the Brodsky lab.


A post-doctoral position is available in our lab. Dr. Brodsky is an Assistant Professor of Pathobiology at the University of Pennsylvania School of Veterinary Medicine, and a member of the Penn Institute for Immunology. The Brodsky lab studies innate immune responses to bacterial infection with a focus on inflammasome biology, cell death signaling pathways, and mechanisms of innate immune evasion by bacterial pathogens. 

See also: http://www.med.upenn.edu/apps/faculty/index.php/g20001900/p8421902

The research community at the University of Pennsylvania provides a dynamic and exciting research environment at the cutting edge of Microbiology and Immunology. A Ph.D. or equivalent in Immunology, Microbiology, Cell Biology, or related field is required. Expertise in innate immunity, multi-parameter flow cytometry, bacterial pathogenesis, biochemistry of innate signaling pathways, and/or host-pathogen interactions is highly desirable.

Please submit a CV and cover letter describing previous research and future research interests along with contact information of three references to ibrodsky@vet.upenn.edu.

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Rotation projects in the Brodsky lab span areas of bacterial physiology and genetics and host innate immune responses. Examples of current rotation projects include:

Project 1: How does intracellular bacterial metabolism influence inflammasome activation? The interaction between intracellular bacterial metabolites and host cell signaling pathways is an emerging area in innate immunity. Our lab recently discovered that altering metabolic flux through the bacterial TCA cycle leads to elevated inflammasome activation in macrophages infected by Salmonella. This project seeks to understand the underlying basis for how disruption of bacterial metabolism results in increased inflammasome activation.

Project 2: How do bacterial pore-forming proteins induce inflammasome activation? Mechanisms of inflammasome activation are an active area of investigation in the field of innate immunity. Our lab has found that the pore forming proteins of bacterial secretion systems trigger inflammasome activation when they are injected into the host cell. New studies in the lab reveal recruitment of these proteins to endosomal membranes. The goal of this project is to understand how this process leads to inflammasome activation.

Project 3: How does apoptosis promote anti-bacterial immunity? Regulation of cell death is critically important for controlling tissue homeostasis and preventing tumorigenesis. Classical apoptosis is viewed as immunomodulatory or immunologically silent. Recent studies have revealed that during bacterial infection, apoptosis promotes specific inflammatory responses that promote control of infection. This project seeks to define the signals released by apoptotic cells that promote activation of anti-bacterial innate and adaptive immune responses.