Academic Seminars

Anthony J.M. Bauer, Ph.D. to present seminar: “Reverse Engineering the Mechanisms of Endotoxin Induced Ileus and its Prevention” on 11/10/17 from 11-12, LIB 110
October 19, 2017
 

Anthony J.M. Bauer, Ph.D., Associate Professor of Physiology, Department of Integrative Physiology and Pharmacology, Liberty University College of Osteopathic Medicine, Lynchburg, VA, will present a seminar entitled: “Reverse engineering the mechanisms of endotoxin induced illus and it prevention”.

Our bacterial residents are Janus-faced deadly indwellers that can lead to a septic-induced systemic inflammatory response syndrome and multiple organ failure. Over half of ICU patients suffer from infections, and sepsis remains one of the top ten causes of death worldwide. Severe ileus frequently accompanies sepsis setting up an insidious cycle of malnutrition, gut-derived microbial translocation and the copious intestinal production of potent systemic inflammatory mediators. Unfortunately, few therapeutic advances have occurred to prevent or treat the sequelae of sepsis. We have pursued a mechanistic “reverse engineering” approach to elucidate the tissue specific signaling pathways associate with Gram-negative endotoxin/TLR4-induced intestinal ileus. These studies have revealed that endotoxin induced ileus is dually mediated by an early MyD88-dependent, non-bone marrow derived mechanism which later combines with classical leukocyte signaling mechanisms. Interestingly, selective intestinal smooth muscle TLR4-dependent responses significantly contribute to the early local molecular inflammatory milieu. However, it appears that the early endotoxin induce ileus is mediated substantially by the induction of an endothelial dependent intestinal microvascular leak syndrome, which triggers the activation of myenteric inhibitory nitrergic motor neurons causing a disruption in normal propulsive gastrointestinal motility. Finally, in preliminary experiments, we sought to employ the transdermal osteopathic-like technique of bowel milking to hypothetically, directly activate enteric anti-inflammatory pathways to ameliorate endotoxin induced ileus.