Inflammatory bowel diseases (IBD), as well as many forms of infectious gastroenteritis, are thought to occur when the integrity of intestinal barriers is disrupted, allowing luminal bacterial products to cross into the intestinal mucosa, stimulating immune cells and triggering and unmitigated immune response. Unfortunately, there is currently no cure, no prevention and limited therapeutic options for IBD. Current evidence suggests that a genetic defect in people with IBD can affect intestinal homeostasis or the balance between an active inflammatory response to an invading pathogen and tolerance to commensal bacteria In individuals with IBD, inflammation is turned on to protect against offending agents, but it doesn’t get turned off once the pathogen has been cleared. Instead, the immune system seems to react to intestinal commensal bacteria that were once tolerated. It is suspected that the usually protective epithelial and mucosal barrier lining the intestine is impaired in patients with IBD, allowing intestinal bacteria to leak across the epithelium and activate immune cells. This prolonged exposure to intestinal bacteria and their products results in exaggerated and chronic inflammation. This causes the symptoms of IBD, which includes diarrhea, severe abdominal pain and other health problems outside the digestive system. Dr. Deanna Gibson is investigating the immune mechanisms involved in IBD by examining how the immune system recognizes and responds to bacteria within the intestine in vivo. She is studying a molecule, Toll-like receptor 2, which has been implicated in IBD and is critical for protecting the intestine from developing severe and lethal colitis. By determining how Toll-like receptor 2 controls susceptibility to bacterial induced colitis, her research could lead to an understanding in intestinal homeostasis which is required to design new therapeutics and discover targets against IBD.