Associate Staff
Email: [email protected]
Location: Cleveland Clinic Main Campus
Our lab studies mechanisms of intestinal health and disease. We are interested in inflammatory bowel disease (IBD), where we investigate ways in which a common carbohydrate polymer, hyaluronan (HA), is produced by cells and in blood vessels during inflammation. We also study ways HA may keep the inflammation going past the point that it is normally healthy, to become destructive to the intestine. Additionally, we are investigating human milk and the natural defense mechanisms turned on by milk carbohydrates, especially HA. Milk HA causes the lining cells of the intestine to produce their own natural antibiotics, and this helps protect from bacterial infection. This mechanism appears to be part of the natural protection passed from mother to baby during breast feeding, but we are trying to devise HA based treatments to protect others with intestinal disease or infection.
Our laboratory focuses innate mechanisms of intestinal protection that when dysregulated lead to disease. Our research focuses on hyaluronan (HA) as a key molecule that mediates the mechanisms, and how, when dysregulated, can lead to disease. We investigate cellular mechanisms pertinent to the inflammatory processes associated with inflammatory bowel disease (Crohn’s disease and ulcerative colitis) and concentrate on altered pathways of extracellular matrix synthesis and catabolism as both cause and effect of inflammation. The etiology of inflammatory bowel disease (IBD), similar to many other inflammatory diseases, is unknown, no doubt because multiple factors are at play to initiate, drive and sustain immune responses. Hyaluronan (HA), an extracellular matrix component, is increased in inflamed human colon during flares of IBD and in animal models of colitis, where it precedes leukocyte infiltration. We are investigating mechanisms through which HA drives and perpetuates inflammation. Additionally, we are investigating human milk and the natural defense mechanisms turned on by milk carbohydrates, especially HA. Milk HA causes the lining cells of the intestine to produce their own natural antibiotics, and this helps protect from bacterial infection. This mechanism appears to be part of the natural protection passed from mother to baby during breast feeding, but we are trying to devise HA based treatments to protect others with intestinal disease or infection.
de la Motte, C, Hascall VC, Calabro, A, Yen-Lieberman, B. and Strong, SA. (1999) J. Biol. Chem. 274:30747-30755 de la Motte, C., Hascall VC, Drazba, J, Bandyopadhyay S, Strong SA. (2003) Am J Path 163:121-133 Day, A.J. and de la Motte, C.A., (2005) Trends in Immunol 26:637-43 Kessler S, Rho H, West G, Fiocchi C, Drazba J, de la Motte C. (2008) Clinical and Translational Sci. 1:57-61. de la Motte C, Nigro J, Vasanji A, Rho H, Kessler S, Bandyopadhyay S, Danese S, Fiocchi C, and Stern R. (2009) Am J Pathol. 174:2254-2264. de la Motte CA and Drazba JA. (2011) J Histochem Cytochem 59:252-257. de la Motte CA. (2011) Am J Physiology-Gastrointestinal and Liver Physiology. 301:G945-9. de Souza HS, West GA, Rebert N, de la Motte C, Drazba J, Fiocchi C. (2012) Gastroenterology 143:1017-26 Hill, DR, Kessler SP, Rho HK, Cowman MK, and de la Motte CA.(2012) J Biol Chem 287: 30610–30624,
Our education and training programs offer hands-on experience at one of the nationʼs top hospitals. Travel, publish in high impact journals and collaborate with investigators to solve real-world biomedical research questions.
Learn MoreInvestigating inter-organ cross-talk between the gut and immune system, Drs. de la Motte and Nagy will test HA35 as potential therapeutic for Western diet-induced metabolic syndrome.