Research Interests

• Intracellular pathogens
• Salmonella
• Bacterial type III secretion
• Endosome trafficking
• Signal transduction

Research Activities 

Salmonella pathogenesis

My research examines how bacteria interact with our cells to cause disease. A major focus of this work is on Salmonella typhimurium, a common cause of food poisoning in North America.

Infections by these bacteria are costly to treat and can be fatal in young children or immunocompromised individuals. Complications of Salmonella infection include reactive arthritis, which leads to the destruction of bone joints. My research examines the molecular mechanisms used by Salmonella to infect host cells and cause disease.

The focus of my work is on toxins known as, 'effectors' that are delivered by the bacteria into host cells using a needle-like delivery system. These effectors have the remarkable ability to manipulate host cell machinery, including signal transduction cascades, cytoskeletal structures and the endosomal system. Upon initial interaction with cells in the gut, a first round of effectors induces uptake of the bacteria into specialized vacuoles. After entering the host cell, a second round of effectors allows Salmonella to replicate inside these niches, eventually killing the infected cell so it can colonize others. The objective of these studies is to determine the molecular mechanisms by which the effectors alter host cell machinery. Through these lines of research, a better understanding of how Salmonella causes disease will be gained.

Autophagy

Autophagy is cellular system that mediates the recycling of cellular components. Recent studies have implicated autophagy in many aspects of cellular physiology, development and responses to stress. Autophagy is also a cellular defence to infection by pathogenic microorganisms. My research examines how autophagy can target bacterial pathogens like Salmonella typhimurium during infection, restricting their growth in host cells. Furthermore we are examining how some bacterial pathogens, like Listeria monocytogenes, can avoid destruction by the autophagy system during infection of host cells.

External Funding

• Canadian Foundation for Innovation
• Ontario Innovation Trust
• Canadian Institutes of Health Research
• Burroughs Wellcome Fund
• Connaught New Staff Matching Grant

Achievements

• Canadian Institutes of Health Research New Investigator Award
• Ontario Premier’s Research Excellence Award (PREA)
• Boehringer Ingelheim Young Investigator Award in Biological Sciences
• Burroughs Wellcome Fund Investigators in Pathogenesis of Infectious Disease Award

Publications

A full list of Dr. Brumell's publications can be found on PubMed.