Karen M. Scanlon, PhD

• National University of Ireland Maynooth, BS, Biology, 2005
• National University of Ireland Maynooth, PhD, Immunology, 2010
• University of Maryland School of Medicine, Postdoctoral Study, Bacteriology & Host Pathogen Interactions, 2013
• University of Maryland School of Medicine, Postdoctoral Study, Host Pathogen Interactions & Bacterial Pathogenesis, 2017

Dr. Scanlon’s research program seeks to define the molecular mechanisms that confer increased infectious disease susceptibility and severity in infants and to use that knowledge for the rational design of host-directed therapeutics. She combines her training in immunology, pulmonary biology, and microbiology to take holistic view of the infection process and delineate age-dependent pathogenic processes that are driven by both pathogen and host.

Dr. Scanlon’s early work identified CCL28, a CC chemokine, as a regulator of IL-17-mediated allergic airway responses and determined the minimum amino acid content required for broad spectrum antimicrobial activity by this protein. While her postdoctoral studies on host-pathogen interactions i) during enteric infection, determined the induction of DNA mutation at colorectal cancer-associated microsatellite instability sites by enteropathogenic Escherichia coli effector proteins and ii) during respiratory infection, identified the host anion exchanger, pendrin, as a major potentiator of Bordetella pertussis-induced pulmonary pathology.

The urgent need for therapeutics to treat severe infant infections such as B. pertussis led Dr. Scanlon to focus her labs efforts on defining and targeting age-dependent host molecules for intervention. She developed an infant mouse model of severe respiratory infection and has used this model to define a number of disease features unique to early life. Dr. Scanlon has utilized an infant mouse pertussis model to determine pertussis toxin-mediated induction of severe disease manifestations such as leukocytosis and pulmonary hypertension during pediatric infection. Due to the unique immune responses and disease susceptibility of infants, these models also provide a rare opportunity to study pathogen shedding and transmission in a wildtype host. Current projects in the lab make use of this platform to investigate immune ontogeny and infection-induced cardiac stress and remodeling in early life. By increasing our understanding of the unique environment pathogens encounter during infant infection, Dr. Scanlon’s work reveals novel targets for the development or repurposing of lifesaving treatments for pediatric infections.  

Immune ontogeny, respiratory infection, pediatric infection, pulmonary hypertension, Bordetella pertussis, pulmonary immunology

Mitchell, A, Scanlon, KM, Flowers, E, Jordan, C, Tibbs, E, Bukowski, A, Gallop, D, Carbonetti, NH (2023) Age-dependent NK cell and interferon-gamma deficits contribute to severe pertussis in infant mice. Journal of Leukocyte Biology 

*Scanlon, KM, Chen, L, Carbonetti, NH (2022) Pertussis toxin promotes pulmonary hypertension in an infant mouse model of Bordetella pertussis. Journal of Infectious Diseases. 224(1): 172-176 [PMID: 34145457] *corresponding author

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) [PMCID: PMC5649019]