Professor of Medicine
Director, Research Center Grant
Our laboratory investigates the cellular and molecular events that occur in the intestine and in response, systemically, to infection with enteric pathogens. Our goal is to understand the mechanisms governing infection-related to intestinal disease and the host defenses against such pathogens as a basis for developing new treatment and preventive strategies.
Two groups of enteric pathogens, Giardia and disease causing Escherichia coli serve as model systems to examine intestinal responses to microbial infection. Giardia is a waterborne protozoan parasite that colonizes the small intestine and attaches to the epithelium, but does not invade the mucosa. Infection is not accompanied by significant mucosal inflammation, yet the host develops effective immune defense and, in most cases, eradicates infection spontaneously. Enteropathogenic E.coli intimately attach to the epithelium and enters the mucosa in modest numbers, processes which are accompanied by significant mucosal inflammation and epithelial hyperplasia. We employ cell and molecular biologic, biochemical, and genetic approaches in murine infection models of Giardia and enteropathogenic E.coli to define the critical immune regulators and effector molecules that control infection with these pathogens and to develop preventive strategies against them.
The other major focus of the laboratory is the pathophysiology of intestinal inflammation. IBD in humans is characterized by chronic, relapsing intestinal inflammation, leading to bouts of diarrhea, abdominal pain, and nutritional deficiencies. Furthermore, chronic inflammation promotes the development of colorectal cancer. The cause of IBD is poorly understood, but inflammation is believe to result from an interaction of the immune system and intestinal bacteria in a genetically susceptible host. Our laboratory employs murine and cell culture models to investigate different aspects of our inflammatory response to microbial and chemical challenges.
Current projects explore the importance of innate immune receptors, specifically toll-like receptors (TLR) and NOD2, and signaling through the NF-kB pathway and cyclic AMP-dependent pathways in controlling intestinal inflammation and colorectal cancer development. Insights from these studies will help us to develop pharmacological strategies to attenuate inflammation and possibly prevent the occurrence of colorectal cancer in IBD patients.
|| Field of Study
| University of Hamburg, Germany
| UCSD, La Jolla, CA
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