Bradley D. Jones, PhD


Professor of Microbiology

Contact Information

Office: 3-330A Bowen Science Building
51 Newton Rd
Iowa City, IA 52242
Phone: 319-353-5457

Lab: 3-330 Bowen Science Building
51 Newton Rd
Iowa City, IA 52242
Phone: 319-335-7794

Email: bradley-jones@uiowa.edu


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

Post Doctorate, Pathogenic Microbiology, Stanford University

Education/Training Program Affiliations

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

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Chen L, Valentine J, Huang C, Endicott C, Moeller T, Rasmussen J, Fletcher J, Boll J, Rosenthal J, Dobruchowska J, Wang Z, Heiss C, Azadi P, Putnam D, Trent M, Jones B, DeLisa M.  Outer membrane vesicles displaying engineered glycotopes elicit protective antibodies.  Proc Natl Acad Sci U S A.  2016 June 28. 113(26):E3609-18.

Wyatt E, Diaz K, Griffin A, Rasmussen J, Crane D, Jones B, Bosio C.  Metabolic Reprogramming of Host Cells by Virulent Francisella tularensis for Optimal Replication and Modulation of Inflammation.  J Immunol.  2016 May 15. 196(10):4227-36.

Roberts L, Crane D, Wehrly T, Fletcher J, Jones B, Bosio C.  Inclusion of Epitopes That Expand High-Avidity CD4+ T Cells Transforms Subprotective Vaccines to Efficacious Immunogens against Virulent Francisella tularensis.  J Immunol.  2016. Epub ahead of print.

Faron M, Fletcher J, Rasmussen J, Apicella M, Jones B.  Interactions of Francisella tularensis with Alveolar Type II Epithelial Cells and the Murine Respiratory Epithelium.  PLoS One.  2015 May 26. 10(5):e0127458.

Rasmussen J, Fletcher J, Long M, Allen L, Jones B.  Characterization of Francisella tularensis Schu S4 mutants identified from a transposon library screened for O-antigen and capsule deficiencies.  Front Microbiol.  2015 May 5. 6:338.

Baxter M, Jones B.  Two-Component Regulators Control hilA Expression by Controlling fimZ and hilE Expression within Salmonella enterica Serovar Typhimurium.  Infect Immun.  2015 March. 83(3):978-85.

Rasmussen J, Post D, Gibson B, Lindemann S, Apicella M, Meyerholz D, Jones B.  Francisella tularensis Schu S4 lipopolysaccharide core sugar and O-antigen mutants are attenuated in a mouse model of tularemia.  Infect Immun.  2014 April. 82(4):1523-39.

Faron M, Fletcher J, Rasmussen J, Long M, Allen L, Jones B.  The Francisella tularensis migR, trmE, and cphA genes contribute to FPI gene regulation and intracellular growth by modulation of the stress alarmone ppGpp.  Infect Immun.  2013 August. 81(8):2800-11.

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.

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.

Date Last Modified: 06/06/2016 - 13:17:48