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Karen M. Scanlon, PhD

Academic Title:

Assistant Professor

Primary Appointment:

Microbiology and Immunology


685 W. Baltimore St. S341

Phone (Primary):

(410) 706-0097

Education and Training

  • National University of Ireland, Maynooth, BSc, Biology, 2005
  • National University of Ireland, Maynooth, PhD, Immunology, 2010
  • University of Maryland School of Medicine, Postdoctoral Study, Microbiology, Mentor: Dr. Michael Donnenberg, 2013
  • University of Maryland School of Medicine, Postdoctoral Study, Microbial Pathogenesis, Mentor: Dr. Nicholas Carbonetti, 2017


Dr. Scanlon's primary research goal is to understand the etiology of age-associated severe disease caused by the respiratory pathogen Bordetella pertussis and to use this knowledge to identify novel therapeutic targets for the treatment of critical pertussis. She started working on respiratory diseases during her graduate studies with Dr. Bernard Mahon, where she determined a role for an antimicrobial chemokine, CCL28, in allergic airway diseases. Subsequent to this, she initiated her postdoctoral studies with Dr. Michael Donnenberg, working on enteropathogenic Escherichia coli effector protein functions, in order to further her understanding of microbial virulence mechanisms. Dr. Scanlon later joined the lab of Dr. Nicholas Carbonetti, where she was able to combine her interests, investigating virulence mechanisms of B. pertussis in the respiratory system.

In her recent work, Dr. Scanlon has focused on the severe manifestation of B. pertussis-induced disease observed in those infected at an early age, termed critical pertussis. Little is known about the pathogenesis of critical pertussis and there are currently limited treatment options. To advance our understanding of critical pertussis, she is further developing a neonatal mouse model of critical pertussis and is using this model as a platform to identify novel age-associated disease mechanisms. With this tool, Dr. Scanlon is investigating the pathogenesis of pulmonary hypertension in critical pertussis, a disease manifestation strongly associated with B. pertussis-induced mortality. She is currently establishing a role for infection-enhanced angiotensin II levels in the muscularization of pulmonary arteries and subsequent increases in pulmonary arterial pressure and heart failure. 

Research/Clinical Keywords

Bordetella pertussis, neonatal infection, pulmonary hypertension, mouse model

Highlighted Publications

  • Scanlon KM, Snyder YG, Skerry C, Carbonetti NH (2017) Fatal pertussis in the neonatal mouse model is associated with pertussis toxin-mediated pathology beyond the airways. Infection & Immunity 85 (11)
  • Skerry C, Scanlon K, Ardanuy J, Roberts D, Zhang L, Rosen H, and Carbonetti NH (2017) Therapeutic treatment with sphingosine-1-phosphate receptor ligands reduces pertussis inflammatory pathology by a pertussis toxin-insensitive mechanism. Journal of Infectious Diseases 215: 278-286
  • Scanlon KM, Skerry C, Carbonetti NH (2015) Novel therapies for the treatment of pertussis disease. Pathogens and Disease 73(8):ftv074 PMCID: PMC4626598
  • Scanlon KM, Gau Y, Skerry C, Soleimani M, Wall SM, and Carbonetti NH (2014) The epithelial anion transporter pendrin contributes to inflammatory lung pathology in Bordetella pertussis infection. Infection & Immunity 82:4212-4221 PMCID: PMC4187853