Each Tuesday, the Daily Voice features a first-person narrative from a researcher explaining the science behind a recent grant, and the inspiration or impetus behind becoming a scientist at UMass Medical School. If you know of a researcher you’d like to see profiled, send an email to UMMScommunications@umassmed.edu.
Beth A. McCormick, PhD, professor of microbiology & physiological systems talks about her recent grant, Intestinal Inflammation Induced by Pathogens, National Institutes of Diabetes and Digestive and Kidney Diseases; one year, $583,453; recommended for four more years, $1.6 million
A major research directive of my laboratory employs enteric pathogens to understand the disease pathophysiology underlying both acute and chronic diseases of the intestinal tract, known as inflammatory bowel disease (IBD). Inflammatory bowel diseases, namely Crohn’s disease and ulcerative colitis, are typically characterized by an abnormal response by the body's immune system, which under normal circumstances protects the body from infection. In people with IBD, however, the immune system reacts inappropriately, mistaking food, bacteria, and other materials in the intestine for foreign or invading substances. As a result, the body “launches an attack” and sends white blood cells into the lining of the intestines, where they produce chronic inflammation. These cells then generate harmful products that ultimately lead to ulcerations and bowel injury, which lead to the clinical manifestations of the disease. We use the enteric pathogens Salmonella typhimurium and Shigella flexneri to understand a fundamental question in IBD: How are these white blood cells directed to the lining of the intestine?
Approximately 7 million patients worldwide suffer from inflammatory bowel disease. The more we understand the process underlying intestinal inflammation, the closer we get to identifying a therapeutic strategy that better controls the recruitment of the white blood cells to sites of gastrointestinal inflammation. Such a strategy would be an attractive means of providing benefit to the millions of patients suffering from these diseases. Toward this objective, we have identified a lipid factor (hepoxilin A3) that is critical in the final step of recruiting white blood cells to these sites of inflammation and have shown that blocking the production of this molecule can dramatically decrease the tissue damage associated with this disease. Founded in our work, a new era of drug discovery for IBD (or other diseases at mucosal surfaces) can be achieved based upon strategies to block the local synthesis and or release of hepoxilin A3 at sites of inflammation.
I have always had an inherent interest in science and discovery, and from a very early age my parents recognized this and have nurtured my scientific curiosity. In elementary school during recess, instead of playing on the jungle gym, I was the kid wondering around the playground with my “geology bag” collecting and identifying different rocks and stone formations. I would then bring the rocks home and polish them up in my rock tumbler, which after a couple of uses was banished to the basement. In later years, my sense of discovery led me to an area of science where many things remain unknown and the science is evolving very quickly.
What drew me to UMMS is the uniquely special scientific community. This community is renowned for the first rate quality of science and for being an institution in which the faculty have a high degree of collaborative spirit and interaction. In addition, UMMS strives to make each faculty member successful by providing a broad spectrum of resources.
What I find most exciting about my job, first and foremost, is that the experiments we think about and perform each day in my lab could, in the future, provide benefit to human health. Personally, there could be no better profession for me to nurture that sense of discovery; and on occasion provide me with an opportunity to play the drums with a band of other scientists (we call ourselves GI Distress) at various conferences.