Enteric bacterial pathogens still remain a global threat to human populations accounting for millions of deaths each year. Pathogenic bacteria are often inadvertently consumed in contaminated food and water supplies resulting in gastroenteric disease. These pathogenic bacteria colonize the human gut, cause acute inflammation and diarrheal illness, followed by shedding into the environment through faecal wastes.
Enteric bacterial pathogens have multiple genetic and biochemical mechanisms that enable them to colonize the human gut, avoid the innate immune response and persist to cause disease. It is hoped that through research we will identify critical bacterial mechanisms involved in disease. Ideally the research findings can be translated into the design of new antimicrobials or inhibitors of these bacterial mechanisms. The overall goal is to reduce the burden of global sickness and suffering caused by enteric pathogens.
To carry out innovative and cutting edge research projects to further advance the understanding of bacterial enteric pathogens
To identify key molecular mechanisms used by enteric pathogens that result in human disease.
My laboratory emphasizes a cross-disciplinary approach to studying host-pathogen interactions, using techniques in the areas of molecular microbiology, genetics, cell biology, immunology, cell structure, signaling, and protein biochemistry. Genomic and proteomic approaches for pathogen profiling have recently resulted in novel discoveries. Fluorescent cell imaging and other microscopy techniques are used to visualize the infection process in vitro.
Extensive actin re-arrangement and hijacking mediated by an effector
protein injected by EPEC during infection. EPEC (stained green) adheres
to intestinal cells and remains extracellular while injecting effector
proteins. In this case, the Tir effector is hijacking host cell actin
(stained in red). This results in an actin rich 'pedestal' structure
underneath adherent EPEC .