Bradley D. Jones, PhD


Professor of Microbiology

Contact Information

Office: 3-330A BSB
Iowa City, IA 52242
Office Phone: 319-353-5457

Lab: 3-330 BSB
Iowa City, IA 52242
Phone: 319-335-7794

Email: bradley-jones@uiowa.edu
Web: BSL-3 Laboratory Facilities


BS, Microbiology, University of Maryland, College Park
PhD, Biochemistry, University of Maryland School of Medicine, Baltimore

Post Doctoral, Pathogenic Microbiology, Stanford University

Education/Training Program Affiliations

Biosciences Graduate Program
Department of Microbiology Graduate Program
Interdisciplinary Graduate Program in Genetics
Medical Scientist Training Program

Research Summary

The Jones laboratory is carrying out research on two different bacterial pathogens, Francisella tularensis and Salmonella spp. Several projects are being pursued with the Select Agent bacterium Francisella tularensis. This organism is a significant biodefense concern because of its extreme pathogenicity and low infectivity. Key advances in our laboratory were the development of genetic systems, including a Tn5 transposition system, which has allowed the creation of bacterial mutants so that various virulence properties of this organism can be deleted and studied. Current work in our laboratory is focused on identifying and characterizing Francisella tularensis mutants with alterations in a variety of virulence mechanisms in this organism including growth and survival in human macrophages, inactivation of human neutrophil responses, entry and growth in primary human small airway epithelial cells and regulation of known and unknown virulence factors. Each of these projects is active and ongoing in the Jones laboratory with collaboration with other laboratories at The University of Iowa.

Other work in the laboratory is focused on understanding the regulators, and the signals that they respond to, in pathogenic Salmonella species. These pathogenic bacteria cause disease in a host by invading epithelial cells of the intestine and subsequently entering and growing within macrophages of the lymphatic system. Salmonella invasion of host cells is accompanied by dramatic changes of the host cell membrane that indicate that these bacteria activate existing cellular signal transduction pathways. The ability of Salmonella to invade host cells is tightly regulated by a number of environmental and genetic signals. One significant project is aimed at understanding how Salmonella establishes colonization of a host intestinal surface (biofilm formation). Recent work from the lab indicates that both extracellular matrix components and adherence factors such as fimbriae play specific and important roles in establishing the extensive biofilm that we observe in the colonization of tissue culture cells and host intestinal tissue. GFP-labelled bacteria are being used to study these events by fluorescent confocal microscopy. Future goals of this work will be aimed at identifying genes involved in the formation of biofilm formation as well as identifying and studying in detail the cells that serve as the attachment sites of the bacteria. In addition, we have developed a genetic screen to identify small molecule inhibitors of various checkpoints in these regulatory cascades which can be disrupted as part of a strategy to intervene in the development of colonization and disease. This work has implications for understanding colonization of Salmonella in domestic animals such as chickens and pigs as well as the establishment of human disease.

Center, Program and Institute Affiliations

Bacterial Respiratory Pathogens Research Unit
Inflammation Program

Selected Publications

Show All

Ulland T, Janowski A, Buchan B, Faron M, Cassel S, Jones B, Sutterwala F.  Francisella tularensis live vaccine strain folate metabolism and pseudouridine synthase gene mutants modulate macrophage caspase-1 activation.  Infect Immun.  2013 January. 81(1):201-8.

Lindemann S, Peng K, Long M, Hunt J, Apicella M, Monack D, Allen L, Jones B.  Francisella tularensis Schu S4 O-antigen and capsule biosynthesis gene mutants induce early cell death in human macrophages.  Infect Immun.  2011 February. 79(2):581-94.

McCaffrey R, Schwartz J, Lindemann S, Moreland J, Buchan B, Jones B, Allen L.  Multiple mechanisms of NADPH oxidase inhibition by type A and type B Francisella tularensis.  J Leukoc Biol.  2010 October. 88(4):791-805.

Ulland T, Buchan B, Ketterer M, Fernandes-Alnemri T, Meyerholz D, Apicella M, Alnemri E, Jones B, Nauseef W, Sutterwala F.  Cutting edge: mutation of Francisella tularensis mviN leads to increased macrophage absent in melanoma 2 inflammasome activation and a loss of virulence.  J Immunol.  2010 September 1. 185(5):2670-4.

Apicella M, Post D, Fowler A, Jones B, Rasmussen J, Hunt J, Imagawa S, Choudhury B, Inzana T, Maier T, Frank D, Zahrt T, Chaloner K, Jennings M, McLendon M, Gibson B.  Identification, characterization and immunogenicity of an O-antigen capsular polysaccharide of Francisella tularensis.  PLoS One.  2010 July 6. 5(7):e11060.

Buchan B, McCaffrey R, Lindemann S, Allen L, Jones B.  Identification of migR, a regulatory element of the Francisella tularensis live vaccine strain iglABCD virulence operon required for normal replication and trafficking in macrophages.  Infect Immun.  2009 June. 77(6):2517-29.

Schulert G, McCaffrey R, Buchan B, Lindemann S, Hollenback C, Jones B, Allen L.  Francisella tularensis genes required for inhibition of the neutrophil respiratory burst and intramacrophage growth identified by random transposon mutagenesis of strain LVS.  Infect Immun.  2009 April. 77(4):1324-36.

Buchan B, McLendon M, Jones B.  Identification of differentially regulated Francisella tularensis genes by use of a newly developed Tn5-based transposon delivery system.  Appl Environ Microbiol.  2008 May. 74(9):2637-45.

Lindemann S, McLendon M, Apicella M, Jones B.  An in vitro model system used to study adherence and invasion of Francisella tularensis live vaccine strain in nonphagocytic cells.  Infect Immun.  2007 June. 75(6):3178-82.

Ledeboer N, Frye J, McClelland M, Jones B.  Salmonella enterica serovar Typhimurium requires the Lpf, Pef, and Tafi fimbriae for biofilm formation on HEp-2 tissue culture cells and chicken intestinal epithelium.  Infect Immun.  2006 June. 74(6):3156-69.

Date Last Modified: 07/31/2013 - 10:51:40