Interest: Influence of stress on innate immune function and wound healing
Previous work has focused on the effects of stress, primarily glucocorticoids, on cutaneous innate immune function and repair. Research in the Radek laboratory focuses on how both physiologic and psychological stress influence cutaneous antimicrobial peptide (AMP) and permeability barrier function in burn and wound injury through activation of acetylcholine nicotinic receptors (nAChR). 1) Psychological stress increases the incidence of infection and delayed healing. Prelimimary studies have demonstrated that nAChR activation significantly suppresses the expression and activity of antimicrobial peptides in skin, leading to greater susceptibility to infection. Current studies are exploring the signaling pathways of nAChR activation associated with this suppression of AMPs and delayed wound repair using mice that are deficient in the nAChR antagonist, Catestatin (Chga -/- mice). Further investigation includes the examination into the regulation and signaling of these receptors in relation to human skin diseases associated with dysregulation of AMPs. 2) Regulation of the cutaneous lipid barrier by nAChR activation is also being investigated. If stress decreases barrier function by nAChR activation, it may be possible to improve or restore normal function of the cutaneous barrier following surgery or injury by using nAChR antagonists. 3) The combination of injury and ethanol significantly increases the risk for morbidity and mortality by negatively impacting multiple systems, including the skin and immune systems, in part, through the activation of the HPA axis. Since ethanol is considered a stress by inducing oxidative stress, the Radek laboratory is exploring the mechanisms by which acute ethanol exposure impairs normal healing in burn and excisional wound models, and whether this occurs through dysregulation of nAChRs and AMPs.
Select Publications
View a partial list of Dr. Radek’s publications through the National Library of Medicine's PubMed online database.
