Steven L. Kunkel, Ph.D.
Professor and Co-Director, Division of General Pathology
Campus Address:
GENERAL PATH M5214 MSI 0602
1301 Catherine Street
Ann Arbor, Michigan 48109-0602
Phone: 734/936-1889
slkunkel@umich.edu
Annual Report | Biography | Research Interests
Departmental Annual Report
Brief Biography
Professor Kunkel earned his undergraduate and M.S. degrees from North Dakota State University, Fargo, North Dakota in 1973 and 1974, respectively, and his Ph.D. (in Microbiology) from the University of Kansas in 1978. He then engaged in Postdoctoral training in Immunopathology at the University of Connecticut Health Center, Farmington, Connecticut from 1978-1980.
In 1980, Dr. Kunkel joined the faculty of the Department of Pathology at the University of Michigan Medical School as an Instructor, was promoted to an Assistant Professor in 1982, Associate Professor in 1986, and Professor of Pathology in 1991. He was awarded the Endowed Professorship in Pathology Research in 1997.
During these years at the University of Michigan, Dr. Kunkel has received significant NIH research support, has been awarded five United States patents, has served on numerous NIH Study Sections, mentored numerous graduate and postdoctoral students, and has engaged in many editorial activities. He is currently the Associate Editor of the Journal of Clinical Investigation, the Senior Associate Editor of the American Journal of Pathology, and the Associate Editor of the Journal of Clinical Immunology.
In addition to these scientific activities, Professor Kunkel has served as the Divisional Director of General Pathology in the Department of Pathology since 1991, and the Associate Dean of the Rackham Graduate School of the University of Michigan since 1995.
Dr. Kunkel’s major research interests involve immunoregulation, inflammatory cell mediator production, and other aspects of molecular biology.
Research Interests
Pathology, Immunoregulation, inflammatory cell mediator production, and molecular biology.
Experimental research activities directed at understanding cytokine networks that are operative in a variety of inflammatory reactions and host defenses represent the major investigative directions of my laboratory. Specific studies are designed to assess the expression and regulation of both proximal mediators, such as interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF) and more distal mediators, such as interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP). Investigations have identified that macrophage-derived IL-1 and TNF can serve as early inflammatory gene products which set in motion a cascade of events, resulting in the expression of chemotactic cytokines (IL-8 and MCP) from a variety of non-immune cells. Fibroblasts, epithelial cell, hepatocytes, and endothelial cells can all express IL-8 and MCP when stimulated with either macrophage condition media, IL-1, or TNF. Steady state levels of IL-8 and MCP mRNA are clearly induced upon stimulation with IL-1 in the pg/ml concentration range.
The ability of non-immune structural cells to express chemotactic cytokines are likely to play a fundamental role in host defense and provide a mechanism for the localization of many acute and chronic inflammatory responses. These chemotactic cytokines may play a key role in the pathology of disease ranging form ischemia/reperfusion injury to chronic allograft rejection.Furthermore, recent studies have inflammation and tumorgenesis. While IL-1 and TNF appear to cause a pro-inflammatory response by initiating cytokine cascades, other cytokines may result in negative effects resulting in the down-regulation of cytokines and their cascades. These latter regulatory polypeptide mediators include interleukin-1 receptor antagonist, IL-4, IL-10, and soluble cytokine receptors. During the evolution of chronic inflammation these signals are likely to mediate the switch between maintenance of the response to resolution of the inflammatory reaction. The Biology of cytokines are studied in the context of an in vitro cellular and molecular approach, as well as in the context of acute and chronic experimental in vivo models of inflammation.