Katherine Radek, PhD

Surgery

Surgical Research
Microbiology and Immunology
Associate Professor

Languages Spoken

English, French

Biography

Interests
Adventure Travels, Astronomy, Yoga, Dogs, Food & Wine, Hiking, Swimming, Animal Shelter Volunteer

Board Certification

American Nurses Credentialing Center
Anesthesiology
American Board of

Research

  • Local Burn Injury Promotes Defects in the Epidermal Lipid and Antimicrobial Peptide Barriers in Human Autograft Skin and Burn Margin: Implications for Burn Wound Healing and Graft Survival Plichta, J. K.; Holmes, C. J.; Gamelli, R. L.; Radek, K. A., Journal of burn care & research : official publication of the American Burn Association
  • Dynamic Role of Host Stress Responses in Modulating the Cutaneous Microbiome: Implications for Wound Healing and Infection Holmes, C. J.; Plichta, J. K.; Gamelli, R. L.; Radek, K. A., Advances in wound care
  • Keratinocyte nicotinic acetylcholine receptor activation modulates early TLR2-mediated wound healing responses Kishibe, M.; Griffin, T. M.; Radek, K. A., International immunopharmacology
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  • Episodic binge ethanol exposure impairs murine macrophage infiltration and delays wound closure by promoting defects in early innate immune responses Curtis, B. J.; Hlavin, S.; Brubaker, A. L.; Kovacs, E. J.; Radek, K. A., Alcoholism, Clinical and Experimental Research
  • Interleukin-33 increases antibacterial defense by activation of inducible nitric oxide synthase in skin Li, C.; Li, H.; Jiang, Z.; Zhang, T.; Wang, Y.; Li, Z.; Wu, Y.; Ji, S.; Xiao, S.; Ryffel, B.; Radek, K. A.; Xia, Z.; Lai, Y., PLoS Pathogens
  • Interplay between Bladder Microbiota and Urinary Antimicrobial Peptides: Mechanisms for Human Urinary Tract Infection Risk and Symptom Severity Nienhouse, V.; Gao, X.; Dong, Q.; Nelson, D. E.; Toh, E.; McKinley, K.; Schreckenberger, P.; Shibata, N.; Fok, C. S.; Mueller, E. R.; Brubaker, L.; Wolfe, A. J.; Radek, K. A., PLoS ONE
  • Local burn injury impairs epithelial permeability and antimicrobial peptide barrier function in distal unburned skin Plichta, J. K.; Droho, S.; Curtis, B. J.; Patel, P.; Gamelli, R. L.; Radek, K. A., Critical care medicine
  • Cholinergic regulation of keratinocyte innate immunity and permeability barrier integrity: new perspectives in epidermal immunity and disease Curtis, B. J.; Radek, K. A., Journal of Investigative Dermatology
  • Sugar-Coating Wound Repair: A Review of FGF-10 and Dermatan Sulfate in Wound Healing and Their Potential Application in Burn Wounds Plichta, J. K.; Radek, K. A., Journal of Burn Care & Research
  • Alcohol exposure and mechanisms of tissue injury and repair Jung, M. K.; Callaci, J. J.; Lauing, K. L.; Otis, J. S.; Radek, K. A.; Jones, M. K.; Kovacs, E. J., Alcoholism, Clinical and Experimental Research
  • Antimicrobial anxiety: the impact of stress on antimicrobial immunity Radek, K. A., Journal of leukocyte biology
  • Acute ethanol exposure disrupts VEGF receptor cell signaling in endothelial cells. Radek, K. A.; Kovacs, E. J.; Gallo, R. L.; DiPietro, L. A., American Journal of Physiology - Heart & Circulatory Physiology
  • Effects of acute ethanol exposure on the early inflammatory response after excisional injury. Fitzgerald, D. J.; Radek, K. A.; Chaar, M.; Faunce, D. E.; DiPietro, L. A.; Kovacs, E. J., Alcoholism: Clinical & Experimental Research
  • Matrix proteolytic activity during wound healing: modulation by acute ethanol exposure. Radek, K. A.; Kovacs, E. J.; DiPietro, L. A., Alcoholism: Clinical & Experimental Research
  • Acute ethanol exposure impairs angiogenesis and the proliferative phase of wound healing. Radek, K. A.; Matthies, A. M.; Burns, A. L.; Heinrich, S. A.; Kovacs, E. J.; Dipietro, L. A., American Journal of Physiology - Heart & Circulatory Physiology
  • Novel function for vascular endothelial growth factor receptor-1 on epidermal keratinocytes. Wilgus, T. A.; Matthies, A. M.; Radek, K. A.; Dovi, J. V.; Burns, A. L.; Shankar, R.; DiPietro, L. A., American Journal of Pathology

Skin Research Interests: Dermatology research in the Radek laboratory focuses on how stress and the cholinergic axis influence cutaneous antimicrobial peptide (AMP) and Toll-like receptor signaling in models of tissue injury and infection in the skin. Antimicrobial peptide (AMP) production is critical for cutaneous homeostasis and the response to injury and infection. Epithelial cells possess a non-neuronal cholinergic system comprised of acetylcholine (ACh) and acetylcholine nicotinic (nAChR) receptors. We previously determined that systemic cholinergic activation via psychological stress in mice diminished epithelial AMP expression, which was restored by topical application of nAChR antagonists. In parallel, we observed an increased susceptibility to Staphylococcal and Streptococcal infection, supporting clinical observations that stress promotes or exacerbates many skin disorders associated with AMP dysregulation. We are investigating how stress and the cholinergic axis may promote AMP dysregulation and subsequent epithelial repair processes in keratinocytes in the context of impaired wound healing, inflammation, and atopic dermatitis. Disrupting this tight balance via changes in AMP regulation can shift the balance to restrict the ability of the skin to combat infection or initiate detrimental inflammatory processes.

Urinary Research Interests: Research in the Radek laboratory focuses on how stress and the cholinergic axis influence antimicrobial peptide (AMP) and Toll-like receptor signaling in the urinary tract. Antimicrobial peptide (AMP) production is critical for epithelial homeostasis and the response to injury and infection. Urothelial cells possess a non-neuronal cholinergic system comprised of acetylcholine (ACh) and acetylcholine nicotinic (nAChR) receptors. We previously determined that systemic cholinergic activation via psychological stress in mice diminished epithelial AMP expression, which was restored by topical application of nAChR antagonists. This association is relevant to the bladder, as several urinary tract disorders (e.g. overactive bladder, painful bladder syndrome) are aggravated by psychological stressors, in part, due to altered nAChR activation. Toll-like Receptors (TLRs) are innate immune receptors that can sense bacterial components to promote AMP induction at the site injury or infection. We recently identified that nAChR activation in urothelial cells dampens TLR2 and TLR4-mediated AMP induction. Thus, we are investigating the mechanisms by which stress and the cholinergic axis may promote AMP dysregulation in urothelial cells in the context of urinary tract infection. Impairment of this pathway is likely a novel cause for recurrent UTI development that contributes to secondary clinical manifestations (i.e. pyelonephritis; urosepsis).

View a partial list of http://www.ncbi.nlm.nih.gov/pubmed/?term=radek+k