Affiliation: UCSD SOM
Associate Professor of Medicine
Phone: 858 534 0683
Lars Eckmann, M.D., is currently Associate Professor in the Department of Medicine at UCSD. Dr. Eckmann received his medical training at the University of Hamburg Medical School in Hamburg, Germany, and conducted additional graduate studies at The Beatson Institute for Cancer Research in Glasgow, Scotland. He performed post-doctoral work at UCSD, and joined the faculty in 1998. He is recipient of several fellowships and awards, including student fellowships from the German Scholarship Foundation and the German Academic Exchange Service, a post-doctoral fellowship and career development award from the Crohn’s and Colitis Foundation of America, and a midcareer investigator award from the National Institutes of Health. During his graduate studies, Dr. Eckmann worked on mechanisms of viral leukemogenesis, while his post-doctoral work and current research focus is in the area of microbial pathogenesis of enteric infections and regulation of inflammation.
Our laboratory conducts research relevant to the understanding of two major groups of human diseases, infections of the intestinal tract with microbial pathogens and inflammatory bowel disease (IBD).
Infections of the gastrointestinal tract with food- and waterborne pathogens are a major health concern in developed countries, and one of the leading causes of death among children in the developing world. Our laboratory investigates the cellular and molecular events that are occur in the intestine and systemically in response to infection with enteric pathogens. The studies have the goal to understand the mechanisms governing infection-related intestinal disease and the host defenses against such pathogens as a basis for developing new treatment and prevention 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 attach intimately to the epithelium and enter 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 prevention 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 believed 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 the 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 new pharmacological strategies to attenuate inflammation and possibly prevent the occurrence of colorectal cancer in IBD patients.
References From PubMed (NCBI)