Update Your ProfileAcademic Title:
Professor
Primary Appointment:
Microbiology and Immunology
Location:
685 W Baltimore St
Phone (Primary):
410-706-7677 (Office)
Phone (Secondary):
410-706-0097 (Lab)
Fax:
410-706-6970
Education and Training
- B.Sc. - Biological Sciences, University of Birmingham, UK (1981)
- Ph.D. - Genetics/Microbiology, University of Leicester, UK (1985)
- Postdoc - Department of Microbiology and Immunology, University of North Carolina at Chapel Hill (Dr. P. Frederick Sparling) (1985-1989)
- European Community Senior Postdoctoral Fellowship - Sclavo Research Center, Siena, Italy (Dr. Rino Rappuoli) (1989-1991)
Biosketch
Dr. Carbonetti started working on pertussis with Dr. Rino Rappuoli at Sclavo Research Centre, Siena, Italy in 1989. In 1991 Dr. Carbonetti was hired to his current position as a faculty member in the Department of Microbiology and Immunology at the University of Maryland School of Medicine in Baltimore. His research is primarily on the basic biology of pertussis infection and disease in mouse models.
Currently his group is investigating mechanisms of disease pathogenesis of Bordetella pertussis infection in adult and infant mouse models, including (i) upregulation of host factors, such as type I and III interferons, in adults that exacerbate lung inflammation, and (ii) deficiency in interferon upregulation in infants that renders them susceptible to lethal disseminating infection. Dr. Carbonetti had the honor of organizing and hosting the ninth International Bordetella Symposium in Baltimore in Sept-Oct, 2010.
Dr. Carbonetti served as program director for the Molecular Microbiology and Immunology graduate program at the University of Maryland School of Medicine from 2005-2015. He has served on the editorial board for the journals Infection & Immunity and Pathogens & Disease and has served on numerous NIH study sections.
Research/Clinical Keywords
Bordetella, pertussis, respiratory infection, host response, lung inflammation, sphingosine-1-phosphate receptor signaling, pendrin, adult and neonatal mouse models, interferons, IL-12
Highlighted Publications
Johnson, D, Carbonetti, N (2023) Roles and effects of interferon lambda signaling in the context of bacterial infections. Journal of Interferon and Cytokine Research 43(9):363-369
Scanlon, KM, Chen, L, Carbonetti, NH (2022) Pertussis toxin-dependent pulmonary hypertension in an infant mouse model of Bordetella pertussis infection. Journal of Infectious Diseases 225(1):172-176Ardanuy, JG, Scanlon, KM, Skerry, C, Fuchs, SY, Carbonetti, NH (2020) Age-dependent effects of type I and type III interferons in the pathogenesis of Bordetella pertussis infection and disease. Journal of Immunology. 204(8):2192-2202
Scanlon, KM, Skerry, C, Carbonetti, NH (2019) Role of major toxin virulence factors in pertussis infection and disease pathogenesis. Advances in Experimental Medicine and Biology 1183:35-51
Scanlon, KM, Skerry, C, Carbonetti, NH (2019) Association of pertussis toxin with severe pertussis disease. Toxins 11, e373
Skerry, C, Dziarski, R, Goldman, WE, Carbonetti, NH (2019) Peptidoglycan recognition protein 4 suppresses early inflammatory responses to Bordetella pertussis and is required for sphingosine-1-phosphate receptor agonist-mediated attenuation of disease. Infection and Immunity 87(2):e00601-18
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:e00355-17
Skerry, C, Scanlon, KM, Ardanuy, JG, Roberts, D, Zhang, L, Rosen, H, Carbonetti, NH (2017) Reduction of pertussis inflammatory pathology by therapeutic treatment with sphingosine-1-phosphate receptor ligands by a pertussis toxin-insensitive mechanism. Journal of Infectious Diseases 215:278-286
Carbonetti, NH (2016) Pertussis leukocytosis: mechanisms, clinical relevance and treatment. Pathogens and Disease 74:ftw087
Plaut, RD, Scanlon, KM, Taylor, M, Teter, K, Carbonetti, NH (2016) Intracellular disassembly and activity of pertussis toxin require interaction with ATP. Pathogens and Disease 74:ftw065
Carbonetti, NH (2015) Contribution of pertussis toxin to the pathogenesis of pertussis disease. Pathogens and Disease 73:ftv073 PMCID: PMC4626579
Additional Publication Citations
Ernst, K, Mittler, A, Winkelmann, V, Kling, C, Eberhardt, N, Anastasia, A, Sonnabend, M, Lochbaum, R, Wirsching, J, Sakari, M, Pulliainen, A, Skerry, C, Carbonetti, NH, Frick, M, Barth, H (2021) Pharmacological targeting of host chaperones protects from pertussis toxin in vitro and in vivo. Scientific Reports 11(1):5429
Locht, C, Carbonetti, NH, Cherry, JD, Damron, FH, Edwards, KM, Fernandez, R, Harvill, ET, Hozbor, D, Mills, KHG, Rodriguez, ME, Mascart, F (2020) Highlights of the 12th International Bordetella Symposium. Clinical Infectious Diseases 71:2521-2526
Carbonetti, NH, Wirsing von König, CH, Lan, R, Jacob-Dubuisson, F, Cotter, PA, Deora, R, Merkel, TJ, van Els, CA, Locht, C, Hozbor, D, Rodriguez, ME (2016) Highlights of the 11th International Bordetella Symposium: From Basic Biology to Vaccine Development. Clinical and Vaccine Immunology 23(11):
Wang, X, Shaw, DK, Hammond, HL, Sutterwala, FS, Rayamajhi, M, Shirey, KA, Perkins, DJ, Bonventre, JV, Velayutham, TS, Evans, SM, Rodino, KG, VieBrock, L, Scanlon, KM, Carbonetti, NH, Carlyon, JA, Miao, EA, McBride, JW, Kotsyfakis, M, Pedra, JHF (2016) The prostaglandin E2-EP3 receptor axis regulates Anaplasma phagocytophilum-mediated NLRC4 inflammasome activation. PLoS Pathogens 12:e1005803 PMCID: PMC4970705
Carbonetti, NH (2016) Bordetella pertussis: New concepts in pathogenesis and treatment. Current Opinion in Infectious Diseases 29:287-294 PMCID: PMC4846492
Guevara, C, Mooi, FR, Greenberg, DP, Decker, MD, Carbonetti, N, Starner, TD, McCray, PB, Iqbal, J, Gómez-Duarte, OG (2016) Primary human airway epithelial cells: a model to study Bordetella pertussis fimbrial-mediated adherence. Infectious Diseases 48:177-188
Scanlon, KM, Skerry, C, Carbonetti, NH (2015) Novel therapies for the treatment of whooping cough. Pathogens and Disease 73:ftv074 PMCID: PMC4626598
Skerry, C, Scanlon, KM, Rosen, H, Carbonetti, NH (2015) Sphingosine-1-phosphate receptor agonism reduces Bordetella pertussis-mediated lung pathology. Journal of Infectious Diseases 211:1883-1886 PMCID: PMC4836722
Scanlon, KM, Gau, Y, Skerry, C, Soleimani, M, Wall, SM, Carbonetti, NH (2014) The epithelial anion transporter pendrin contributes to inflammatory lung pathology in Bordetella pertussis infection. Infection & Immunity 82:4212-4221 PMCID: PMC4187853
Connelly, C, Sun, Y, Carbonetti, NH (2012) Pertussis toxin exacerbates and prolongs airway inflammatory responses during Bordetella pertussis infection. Infection & Immunity 80:4317-4332 PMCID: PMC3497438
Worthington, ZEV, van Rooijen, N, Carbonetti, NH (2011) Enhancement of Bordetella parapertussis infection by Bordetella pertussis in mixed infection of the respiratory tract. FEMS Immunology and Medical Microbiology 63:119-128 PMCID: PMC3170498
Ayala, VI, Teijaro, JR, Farber, DL, Dorsey, SG, Carbonetti, NH (2011) Bordetella pertussis infection exacerbates influenza virus infection through pertussis toxin-mediated suppression of innate immunity. PLoS ONE 6(4): e19016 PMCID: PMC3080395
Research Interests
We are interested in the pathogenesis of infection and disease caused by Bordetella pertussis, the agent of pertussis or whooping cough. We use adult and infant animal models and in vitro approaches to investigate this host-pathogen interaction, with an emphasis on the host response and age-dependent outcomes. Current projects include the following:
- Role of interferons in lung inflammatory pathology caused by Bordetella pertussis infection in adult mice. We identified the type I and III IFN receptors as significant activators of lung inflammatory responses during peak B. pertussis infection. We are studying the activation of type I and III IFN expression and their link to lung inflammatory pathology through effects on neutrophils in adult mouse models.
- Neonatal mice infection with Bordetella pertussis as a model of critical pertussis in human infants. As in humans, neonatal mice are susceptible to fatal B. pertussis infection. We found that this lethality is completely dependent on PT activity and that the pathogenesis of disease is quite different from that caused by B. pertussis infection in adult mice. Lack of induction of type I, II and III interferons in response to infection in these mice contributes to susceptibility to lethal disseminating infection. We are studying age-dependent host responses and their role in protection against lethal pertussis infection.
Grants and Contracts
NIH/NIAID R21 AI156042 NK cell and interferon gamma deficiency in infant susceptibility to pertussis 3/10/21 - 2/28/23 (PI: Carbonetti, NH)
NIH/NIAID R01 AI141372 Age-dependent role of type I interferon in Bordetella pertussis pathogenesis 9/19/18 - 8/31/23 (PI: Carbonetti, NH)
Professional Activity
- 2019: Scientific Organizing Committee, 12th International Bordetella Symposium, Brussels, Belgium, April 9-12, 2019 - Chair, Immune Responses session2018-2019: President, Maryland Branch, American Society for Microbiology
- 2017-2019: Deputy Editor-in-chief, Pathogens and Disease
- 2017: Chair, ZGM1 MBRS-SCORE Study Section, NIH
- 2016: Scientific Organizing Committee, 11th International Bordetella Symposium, Buenos Aires, Argentina, April 5-8, 2016 – Chair, Immune Responses session; Chair, Pertussis Vaccines Roundtable Discussion session
- 2014: Chair, ZGM1 MBRS-SCORE Study Section, NIH
- 2013-2019: Editor, Pathogens and Disease
- 2010: Organizing Committee Chair and Host, 9th International Bordetella Symposium, Baltimore, MD, Sept 30 - Oct 3, 2010
- 2009-2020: Editorial Board Member, Infection and Immunity