Professor of Pathology
Director, UAB Medical Scientist Training Program
| Address: | 1825 University Blvd Shelby Bldg, room 121C UAB Birmingham, AL 35294 |
| Telephone: | (205) 934-0676 |
| Email: | rlorenz@uab.edu |
| Publications |
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Education
B.S. (Biology), Stanford University, Stanford, CA
M.D. Washington University, St. Louis, MO
Ph.D. Washington University, St. Louis, MO
Residency (Clinical Pathology), Barnes Hospital, St. Louis, MO
Research Interests
The focus of research in our laboratory is the study of the cellular components of the mucosal immune system and their interactions with the gastrointestinal epithelium, the GI microbiome, and the systemic immune response. Our first area of interest is the cellular immune response to Helicobacter in a mouse model of gastric infection and inflammation. The bacteria Helicobacter pylori is a major pathogen which is linked to acute and chronic gastritis and adenocarcinoma. It is also linked to protection from esophageal cancers and allergic asthma. We are currently investigating the interactions between gastric Helicobacter infection and asthma susceptibility in a mouse model of lung inflammation.
The second area of focus in our laboratory is the role of the intestinal epithelium and innate immune responses in the development of inflammatory bowel disease (IBD). The chronic intestinal inflammation that characterizes IBD is the result of a poorly controlled mucosal immune response to normal intestinal microbiota. The mechanisms that initiate this aberrant response are not well elucidated; however, one possibility is that a change in the intestinal epithelial barrier results in increased systemic exposure to microbial products. The P-glycoprotein (mdr1a-/-) deficient mouse is a unique model of spontaneous colitis that demonstrates an increase in colonic epithelial permeability, as well as a change in the sensitivity of toll-like receptors (TLRs) to bacterial products. Our laboratory focuses on investigating the relationships between the membrane pump- P-glycoprotein, microbial sensors-such as TLRs, and IBD. These studies utilize both in vivo models of IBD, as well as in vitro primary and continuous epithelial cell culture systems. The understanding of the basic mechanisms by which the host maintains intestinal homeostasis and barrier integrity will lay the foundation for future studies on the regulation of the inflammatory response and the design of therapies for human IBD.
The third focus of our laboratory is the influence of mucosal immune factors on the risk of type 1 diabetes development. The incidence of autoimmune Type I Diabetes (T1D) in both human patients and animal models is altered by genetic and environmental factors. These factors include an increased incidence after exposure to high fat diets and hygienic environments. These environmental effects are reproduced in the NOD mouse model of disease, where animals raised in a sterile environment have an increased incidence of disease. In addition to diabetic effects, these environmental exposures have in common the fact that they alter two components of the gastrointestinal (GI) ecosystem, the resident microbiota and the intestinal immune response. Our research focuses on the interrelationship between the GI microbiota, the intestinal immune response, and the risk of T1D development in the NOD mouse model.