Loyola University Chicago
Katherine A. Radek, PhD – Associate Professor of Surgery. Loyola University Chicago, Health Sciences Campus
Dr. Radek’s research program investigates the mechanisms by which physiologic stressors and cholinergic signaling impair normal skin barrier function and wound repair processes through defects in the innate immune response, including antimicrobial peptides (AMPs), Toll-like receptors (TLRs), and the bacterial microbiome. Her laboratory discovered that keratinocyte 7 nicotinic acetylcholine receptor (nAChR) activation elicits an immunosuppressive response via suppression of AMPs, resulting in a greater risk for skin infection. However, little is known about the mechanisms by which nAChR activation influences wound inflammation and microbial susceptibility. Dr. Radek’s lab determined that topical nAChR activation treatment reduced wound TLR2 levels, which resulted in increased bacterial survival and delayed healing in normal wounds in vivo. However, topical nAChR activation reduced wound TLR2 S. aureus MRSA survival and dissemination in a mouse model of chronic wound infection. This suggests that topical nAChR agonists may be used as novel therapeutics to control inflammation and/or infection in chronic, non-healing wounds. Her laboratory also identified We recently reported that burn injury dysregulates several key skin barrier function elements, including barrier protein expression, trans-epidermal water loss, cytokines and antimicrobial peptides (AMPs). AMPs are conserved innate immunity components that help regulate skin barrier homeostasis and protection from infection in both mice and humans. We also identified skin bacterial microbiome dysbiosis after burn in humans, which correlated with the increased burn wound infection risk and sepsis. Her laboratory has developed and utilized various transgenic animal models in models of wound healing and bacterial infection, has employed human tissue from burn and chronic wound patients. The ultimate goal of Dr. Radek’s studies is to identify novel pathways as target for pharmacologic intervention in order to promote optimal wound healing and reduce infection risk in burn and chronic wound patients.