SOM Faculty Profile : Nicholas H Carbonetti

Nicholas H Carbonetti

Nicholas H Carbonetti Ph.D.

Academic Title: Associate Professor

Primary Appointment: Microbiology and Immunology

ncarbone@umaryland.edu

Location: HSF 1 325 B

Phone: 410-706-7677 (Office)

Phone: 410-706-0097 (Lab)

Fax: 410-706-2129

Research Interests

The general interest in my laboratory includes (i) molecular and cellular mechanisms of bacterial pathogenicity, (ii) immune and inflammatory responses to bacterial infection, and (iii) cell biology of bacterial toxins. Specifically, we are studying the role of virulence factors in infection and disease caused by the bacterial pathogen Bordetella pertussis, the cause of the disease whooping cough or pertussis. We are using a mouse model of respiratory tract infection to study this host-pathogen interaction, and we are particularly interested in the role played by the secreted virulence factor pertussis toxin and its modulatory effects on the host immune response. We are also studying the retrograde transport in mammalian cells of pertussis toxin, and the intracellular trafficking pathway that this toxin utilizes to arrive at and modify its target G proteins, disrupting cell signaling events and causing toxicity. We are using various cell biology approaches to dissect this pathway and learn about the intracellular events that lead to pertussis toxin activity.

Publications

Andreasen, C, and Carbonetti, NH (2009) The role of neutrophils in response to Bordetella pertussis infection in mice. Infection & Immunity 77: 1182-1188

Andreasen, C, Powell, DA, and Carbonetti, NH (2009) Pertussis toxin stimulates IL-17 production in response to Bordetella pertussis infection in mice. PLoSONE 4(9): e7079

Plaut, RD, and Carbonetti, NH (2008) Retrograde trafficking of pertussis toxin in mammalian cells. Cellular Microbiology 10:1130-1139

Andreasen, C, and Carbonetti, NH (2008) Pertussis toxin inhibits early chemokine production to delay neutrophil recruitment in response to Bordetella pertussis respiratory tract infection in mice. Infection & Immunity 76:5139-5148

Carbonetti, NH (2007) Immunomodulation in the pathogenesis of Bordetella pertussis infection and disease. Current Opinion in Pharmacology 7:272-278

Worthington, ZEV, and Carbonetti, NH (2007) Evading the Proteasome: Absence of lysine residues contributes to pertussis toxin activity by evasion of proteasome degradation. Infection & Immunity 75:2946-2953

Carbonetti, NH, Artamonova, GV, van Rooijen, N, and Ayala, VI (2007) Pertussis toxin targets airway macrophages to promote Bordetella pertussis infection of the respiratory tract. Infection & Immunity 75:1713-1720

Carbonetti, NH, Mays, RM, Artamonova, GV, Plaut, RD and Worthington, ZEV (2005) Proteolytic cleavage of pertussis toxin S1 subunit is not essential for its activity in mammalian cells. BMC Microbiology 5:7

Carbonetti, NH, Artamonova, GV, Andreasen, C, and Bushar, N (2005) Pertussis toxin and adenylate cyclase toxin provide a one-two punch for establishment of Bordetella pertussis infection of the respiratory tract. Infection & Immunity 73:2698-2703

Carbonetti, NH, Artamonova, G, Andreasen, C, Dudley, E, Mays, RM, and Worthington, ZEV (2004) Suppression of serum antibody responses by pertussis toxin after respiratory tract colonization by Bordetella pertussis and identification of an immunodominant lipoprotein. Infection & Immunity 72:3350-3358

Carbonetti, NH, Artamonova, G, Mays, RM, and Worthington, ZEV (2003) Pertussis toxin plays an early role in respiratory tract colonization by Bordetella pertussis. Infection & Immunity 71:6358-6366

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