Dr. Lenard M. Lichtenberger
The University of Texas at Houston
Department of Integrative Biology and Pharmacology
- Mechanism of peptic ulcer disease
The gastrointestinal mucosa is constituted by a population of highly differentiated epithelial cells that have secretory, absorptive and endocrine functions. The luminal surface of these polarized epithelial cells interface with a hostile proteolytic environment that will readily digest dietary nutrients. To prevent autolysis, the gastrointestinal mucosa developed intricate barrier properties, that prevent the back-diffusion of luminal acid, bacterial toxins and other agents (e.g. bile salts). This barrier property, is compromised in disease states leading to peptic ulcer disease and other erosive diseases of the GI tract. Our laboratory has been studying the surface barrier properties of the stomach in healthy and disease states both in clinical tissue and in animal models of peptic ulcer disease and colitis. We have determined that the mucus gel layer of both the gastric and colonic mucosa have unique hydrophobic or non-wettable properties that protect the underlying tissue from noxious water-soluble agents in the lumen. Furthermore, we have demonstrated that this biophysical property is attributable to the ability of surface mucus cells to biosynthesize and secrete surfactant-like phospholipids that recruit to the air/liquid interface of the mucus gel layer. We have also demonstrated that this hydrophobic phospholipid layer is attenuated in conditions associated with peptic ulcer disease (intake of aspirin and other non-steroidal anti-inflammatory drugs/NSAIDs and infection with Helicobacter pylori in both man and animal models). We are presently utilizing this information to develop strategies to fortify the barrier to treat/prevent peptic ulcer disease.
Program in Cell and Regulatory Biology (Pharmacology and Physiology Tracks)
Office: MSB 4.222
Ph.D. - University of Oklahoma Medical School - 1972