Kevin Mason, Ph. D. :: Nationwide Children's Hospital, Columbus, Ohio

Kevin Mason, PhD

Kevin  Mason, PhD

Center for Microbial Pathogenesis
Principal Investigator

Kevin Mason Lab
Principal Investigator

Contact Information

The Research Institute at Nationwide Children's Hospital
700 Children's Drive, W531
Columbus, Ohio 43205 [ map ]
PH: (614) 355.3534
FX: (614) 722.2818
Email Me


Kevin Mason, PhD, is an Assistant Professor of Pediatrics at The Ohio State University School of Medicine in the Center for Microbial Pathogenesis, The Research Institute at Nationwide Children’s Hospital.

The Mason laboratory studies pathogenic mechanisms that equip survival of nontypeable Haemophilus influenzae (NTHi) during transition from a commensal microorganism of the nasopharynx to pathogen of the upper and lower airways. Of critical importance is the ability of NTHI to adapt to host microenvironments, specifically the limitation of nutrients and host immune pressures. The lab has identified mechanisms of innate immune resistance and nutrient uptake that are essential for NTHI pathogenesis. The lab's work is focused on three main areas of investigation: 1) how host nutritional immunity influences NTHI biofilm architecture via morphological changes in bacteria, invasion of host epithelial cells and modulation of inflammatory responses that contributes to persistence and disease severity; 2) Sap-transporter mediated uptake of nutrients and host derived antimicrobial peptides as a mechanism of survival; 3) biochemical analysis of Sap ABC transporter assembly and function in response to host nutritional and innate immune pressures. Elucidation of mechanisms of pathogenesis will allow the lab to develop and apply novel strategies to target NTHI virulence mechanisms.

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  • Male

Languages Spoken:

  • English

Research Interests

Research Center:

Areas of Interest:

  • Studies in my laboratory focus on understanding the complex molecular mechanisms that underlie bacterial pathogenesis and the host response. Nontypeable Haemophilus influenzae (NTHi) is a common member of the host normal flora (a commensal) and yet predominates in both chronic otitis media with effusion, acute otitis media and in other localized respiratory diseases such as acute sinusitis, community-acquired pneumonia and has important consequences in patients with chronic obstructive pulmonary disease and cystic fibrosis (opportunistic pathogen). We hypothesized that NTHi differentially expresses a number of genes as the microbe transitions to an opportunistic disease state. Our investigations provided one of the earliest description and understanding of Haemophilus pathogenesis in vivo. Importantly, NTHI adaptation to the diverse host environment resulted in the up-regulation of sap (sensitivity to antimicrobial peptides) operon gene expression, previously shown in other microorganisms to mediate resistance to killing by antimicrobial peptides (APs), key components of the host innate immune response. These genes encode the Sap transporter, a member of an ABC transporter family that mediates recognition of small peptides, cations, or iron-containing proteins, which are then targeted for transport across the inner membrane into the bacterial cytoplasm. We hypothesized that the pathogenic potential of NTHI is dictated by its ability to resist immune-mediated clearance mechanisms and specifically, killing by host APs. Using genetic tools and biophotonic imaging of NTHi-infected chinchillas, we demonstrated that the sap genes are expressed in vivo early in infection and mutants defective in sap gene expression are sensitive to killing by host APs, and thus, are rapidly cleared in vivo. Our work showed that APs directly bind the Sap transporter binding protein, supporting a model of AP transport to the bacterial cytoplasm and subsequent proteolysis or destruction, and initiation of a regulatory cascade that activates other resistance determinants. We further demonstrated that components of the Sap transporter are also required for potassium uptake in NTHi, a function which counters rapid potassium efflux from the bacterium, a hallmark of AP lethality. Current work in my laboratory continues to define how NTHI senses and transports APs, and define a role for Sap proteins in ATP-dependence on potassium transport, thus supporting a dual molecular mechanism that promotes bacterial survival and establishment of disease. Further, we are interested in the role Sap gene products play in NTHi survival on epithelial cells since mutations in the Sap transporter alter NTHi biofilm formation, adherence properties and alter host cell responses. Since Sap system homologues are conserved among bacterial species, our long-range goal is to better define a global resistance mechanism which, if targeted, could have far-reaching implications and therapeutic value. Lab Web Site:

Education and Training

Undergraduate School

  • The Ohio State University
    Date Completed: 06/30/1992


  • Wright State University
    Date Completed: 06/30/1998

Post Doctoral

  • Duke University
    Date Completed: 06/30/2000

Post Doctoral

  • The Research Institute, Nationwide Children's Hospital
    Date Completed: 06/30/2006

Professional Experience


  • Assistant Professor of Pediatrics, The Ohio State University


  • Pettigrew M.M., Alderson M.R., Bakaletz L.O., Barenkamp S.J., Hakansson A.P., Mason K.M., Nokso-Koivisto J., Patel J., Pelton S.I. and Murphy T.F. 2016. Panel 6: Vaccines.  Otolaryngology: Head and Neck Surgery. Vol. 1, no. July: e1.
  • Horvath Jr. D.J., Patel A.S., Mohamed A., Storm D.W., Singh C., Li B., Zhang J., Koff S.A., Jayanthi V.R., Mason K.M. and Justice S.S. 2016. Association of O-Antigen Serotype with the Magnitude of Initial Systemic Cytokine Responses and Persistence in the Urinary Tract.  Journal of Bacteriology. Vol. 198, no. 6. (March): 964-972.
  • Harrison A., and K.M. Mason. 2016. Pathogenesis of Haemophilus influenzae in humans. In Emerging and Re-Emerging Human Infections. Edited by S.S. Singh. Hoboken: John Wiley & Sons/Wiley Blackwell Press.
  • Harrison A., Dubois L.G., St John-Williams L., Moseley M.A., Hardison R.L., Heimlich D.R., Stoddard A., Kerschner J.E., Justice S.S., Thompson J.W. and Mason K.M. 2016. Comprehensive proteomic and metabolomic signatures of nontypeabble Haemophilus influenzae-induced acute otitis media reveal bacterial aerobic respirartion on an immunosuppressed environment.  Molecular Cell Proteomics. Vol. 15, no. 3. (March): 1117-1138.
  • Sun D., Crowell S., Harding C.M., Fernando D.M., Mason K.M., Harrison A., Loewen P.C., Kumar A. and Liu Y. 2016. KatG and KatE confer Acintobacter resisitance to hydrogen peroxide but sensitize bacteria to killing by phagocytic respiratory burst.  Life Sciences. Vol. 148, no. March: 31-40.
  • Heimlich D.R., Harrison A. and Mason K.M. 2014. Host antimicrobial peptides in bacterial homeostasis and pathogenesis of disease.  Antibiotics. Vol. 3, no. 4. (December): 645-676.
  • Justice,Sheryl,S; Harrison,Alistair; Becknell,Brian; Mason,Kevin,M. 2014. Bacterial differentiation, development, and disease: mechanisms for survival.  FEMS MICROBIOLOGY LETTERS. Vol. 360, no. 1. (November): 1-8.
  • Justice S.S., Harrison A., Beckness B. and Mason K.M. 2014. Bacterial differentiation, development and disease: mechanisms for survival.  FEMS Microbiology Letters. Vol. 360, no. 1. (November): 1-8.
  • Szelestey B.R, Heimlich D.R., Raffel F.K., Justice S.S. and Mason K.M. 2013. Haemophilus Responses to Nutritional Immunity: Epigenetic and Morphological Contribution to Biofilm Architecture, Persistence and Disease.  PLoS Pathogens. Vol. 9, no. 10. (October): ee1003709.
  • Harrison A., Santana E.A., Szelestey B.R., Newsom D.E., White P. and Mason K.M. 2013. Ferric uptake regulator and its role in the pathogenesis of nontypeable Haemophilus influenzae.  Infection and Immunity. Vol. 81, no. 4. (April): 1221-1233.
  • Cave-Thomasen P., Hermansson A., Bakaletz L., Hellstrom S., Kanzaki S., Kerschner J., Lin D., Mason K. and Spratley J. 2013. Panel 3: Recent advances in anatomy, pathology and cell biology in relation to otitis media pathogenesis.  Otolaryngol Head Neck Surg. Vol. 148, no. (Suppl 4). (April): E37-51.
  • Caye-Thomasen P., Hermansson A., Bakaletz L., Hellstrom S., Kanzaki S., KerschnerJ., Lim D., Lin J., Mason K. and Spratley J. 2013. Panel 3: Recent Advances in Anatomy, Pathology, and Cell Biology in Relation to Otitis Media Pathogenesis.  Otolaryngology: Head and Neck Surgery. Vol. 148, no. April: E37-E51.
  • Raffel F.K., Szelestey B.R., Beatty W.L. and Mason K.M. 2013. The Haemophilus influenzae Sap transporter mediates bacterium-epithelial cell homeostasis.  Infection and Immunity. Vol. 81, no. 1. (January): 43-54.
  • Vogel A.R., Szelestey B.R., Raffel F.K., Sharpe S.W., Gearinger R.L., Justice S.S. and Mason K.M. 2012. SapF-mediated heme-iron utilization enhances persistence and coordinates biofilm architecture of Haemophilus.  Frontiers in cellular and infection microbiology. Vol. 2, no. January: e42.
  • Shelton, C.L., Raffel, F.K., Beatty, W.L., Johnson, S.M. and Mason K.M. 2011. Sap transporter mediated import and subsequent degradation of antimicrobial peptides in Haemophilus.  PLoS Pathogens. Vol. 7, no. 11. (November): eE1002360.
  • Sharpe S.W., Kuehn M.J. and Mason K.M. 2011. Elicitation of epithelial-derived immune effectors by outer membrane vesicles of nontypeable Haemophilus influenzae.  Infection and Immunity. Vol. 79, no. August: 4361-4369.
  • Mason K.M., Raffel F.K., Ray C.W. and Bakaletz L.O. 2011. Heme utilization by nontypeable Haemophilus influenzae is essential and dependent on Sap transporter function.  Journal of Bacteriology. Vol. 193, no. 10. (January): 2527-2535.
  • McGillivary G., Mason K.M., Jurcisek J.A., Peeples M.E. and Bakaletz L.O. 2009. Respiratory syncytial virus-induced dysregulation of expression of a mucosal beta-defensin augments colonization of the upper airway by non-typeable Haemophilus influenzae.  Cellular Microbiology. Vol. 11, no. 9. (September): 1399-1408.
  • Kerschner J.E., Kawauchi H., Alper C.M., Lee H.Y., Stenfeldt K., Bakaletz L, Hellstrom S.O., Herman P., Hussl B., Iino Y., Mason K., Jung T., Chole R.A., Lim D.J., Lin J. and Paparella M. 2007. Panel 3: Pathogenesis: Anatomy and Pathology, and cell biology.  Recent Advances in Otitis Media. Vol. 1, no. April: e40.
  • Hong W., Mason K.M., Jurcisek J.A., Novotny L.A., Bakaletz L.O. and Swords W.E. 2007. Phosphorylcholine decreases early inflammation and promotes establishment of stable biofilm communities of NTHI strain 86-028NP in a chinchilla model of otitis media.  Infection and Immunity. Vol. 2, no. 75. (January): 958-965.
  • Mason K.M., Bruggeman M.E., Munson R.S., Bakaletz L.O. 2006. The non-typeable Haemophilus influenzae Sap transporter provides a mechanism of antimicrobial peptide resistance and SapD-dependent potassium acquisition.  Molecular Microbiology. Vol. 62, no. 5. (December): 1357-1372.
  • Mason K.M., Munson R.S. Jr, Bakaletz L.O. 2005. A mutation in the sap operon attenuates survival of nontypeable Haemophilus influenzae in a chinchilla model of otitis media.  Infection and Immunity. Vol. 73, no. 1. (January): e599.
  • Novotny L.A., Mason K.M. and Bakaletz L.O. 2005. Development of a chinchilla model to allow direct, continuous, biophotonic imaging of bioluminescent nontypeable Haemophilus influenzae during experimental otitis media.  Infection and Immunity. Vol. 73, no. 1. (January): e609.
  • Kesty N.C., Mason K.M., Reedy M., Miller S.E. and Kuehn M.J. 2004. Enterotoxigenic Escherichia coli vesicles target toxin delivery into mammalian cells.  The EMBO Journal. Vol. 23, no. 23. (November): e4538.
  • Mason K.M., Munson R.S. Jr. and Bakaletz L.O. 2003. Nontypeable Haemophilus influenzae gene expression induced in vivo in a chinchilla model of otitis media.  Infection and Immunity. Vol. 71, no. 6. (June): e3454.
  • Mason K.M., Dryden T.D., Bigley N.J. and Fink P.S. 1998. Staphylococcal enterotoxin B primes cytokine secretion and lytic activity in response to native bacterial antigens.  Infection and Immunity. Vol. 66, no. 11. (November): e5082.
  • Curiel R.E., Mason K.M., Dryden T.D., Maurer M.J. and Bigley N.J. 1998. Cytokines produced early in picornavirus infection reflect resistance or susceptibility to disease.  Journal of Interferon & Cytokine Research: The Official Journal of The International Society for Interferon and Cytokine Research. Vol. 18, no. 8. (August): e587.
  • Mason K.M., Bigley N.J. and Fink P.S. 1998. Development of a novel in vitro co-culture system for studying host response to native bacterial antigens.  Journal of Immunological Methods. Vol. 211, no. 1-2. (February): e147.

Awards, Honors and Organizations

  • THE LEADERSHIP AWARD, Department of Pediatrics 2013 Junior Faculty Award - The Ohio State University College of Medicine, Department of Pediatrics
Nationwide Children's Hospital
700 Children's Drive Columbus, Ohio 43205 614.722.2000