Paul M. Guyre, PhD
Active Emeritus Professor of Microbiology and Immunology
Microbiology and Immunology
Montclair State College, BA 1972
U. New Hampshire, PHD 1979
U. New Hampshire, MS 1976
Molecular and Cellular Biology Graduate Programs
Norris Cotton Cancer Center
Program in Experimental and Molecular Medicine
Geisel School of Medicine at Dartmouth
Lebanon NH 03756
Phone: 603 650-7924
Dr. Guyre's principal research interest is understanding how hormones and cytokines regulate the functional activity of white blood cells including monocytes, macrophages, dendritic cells, and neutrophils. The goal of Dr. Guyre's current research is to elucidate the physiologic interactions between steroid hormones that often regulate immune responses and molecules that activate the immune system such as cytokines and interferons. For example, bacterial infections stimulate the production of cytokines that activate leukocytes, but also feed back via the brain and pituitary to stimulate the release of cortisol from the adrenal gland. Cortisol (as well as related steroids that are used therapeutically as anti-inflammatory agents) then interacts with cytokines to either enhance or inhibit leukocyte activation as needed. Together with collaborators Drs. Pioli, Yeager and Wira,, Dr. Guyre's research team is identifying the mechanisms by which leukocyte receptors and signaling pathways are regulated by hormones and cytokines to enhance the killing of pathogens and/or suppress inflammation in sepsis, autoimmunity and cardiovascular disease.
Advanced Biomedical Sciences
After Dr. Guyre received his Ph.D from the University of New Hampshire in 1978, he trained as a postodoctoral research associate with Allan Munck in the DMS Department of Physiology. He joined the Physiology faculty in 1980, and has been a Professor of Physiology and of Microbiology/Immunology since 1991.
The Stress Hormone Cortisol Enhances Interferon-υ-Mediated Proinflammatory Responses of Human Immune Cells.
Glucocorticoids enhance the in vivo migratory response of human monocytes.
A subset of human uterine endometrial macrophages is alternatively activated.
Cortisol exerts bi-phasic regulation of inflammation in humans.
Hydrocortisone at stress-associated concentrations helps maintain human heart rate variability during subsequent endotoxin challenge.
Human uterine epithelial cell secretions regulate dendritic cell differentiation and responses to TLR ligands.
Estradiol suppresses NF-kappa B activation through coordinated regulation of let-7a and miR-125b in primary human macrophages.
Pretreatment with stress cortisol enhances the human systemic inflammatory response to bacterial endotoxin.
Estradiol regulates expression of estrogen receptor ERalpha46 in human macrophages.
Functional expression of pattern recognition receptors in tissues of the human female reproductive tract.