Microbiology

Blaise R. Boles, PhD

Portrait

Assistant Professor of Microbiology

Contact Information

Office: 3-550 Bowen Science Building
51 Newton Road
Iowa City, IA 52242
Office Phone: 319-335-8807

Lab: 3-501K Bowen Science Building
51 Newton Rd
Iowa City, IA 52242

Email: blaise-boles@uiowa.edu
Web: Boles Lab Website
Web: Google Scholar Page
Web: Boles Lab on Twitter

Education

BS, Microbiology, University of Iowa
MS, Microbiology, University of Iowa
PhD, Microbiology, University of Iowa

Post Doctoral, Microbiology, University of Iowa

Education/Training Program Affiliations

Biosciences Graduate Program
Medical Scientist Training Program

Research Summary

The Boles lab utilizes molecular, genetic, biochemical, and ecological approaches to understand the microbial ecology of humans. Only one in ten of the cells constituting a human being is mammalian – the rest are microbes and small multicellular organisms. The association between these microbes and mammalian cells is a living structure that we think of as the human body. One can think of our bodies as complex ecosystems that provide a variety of environments - each of which is populated by a distinct microbial community. These complex communities of microorganisms associated with the human body plays a key role in health and disease. Our vision is to gain knowledge about how bacteria colonize, persist in, and disperse from these human ecosystems and transfer this knowledge to better diagnosis, treat, and prevent infectious disease.

Staphylococcus aureus is a human commensal that commonly lives in our noses and on our skin and much of our current research focus centers around this bacterium. When given the opportunity to enter our bodies S. aureus can be a dangerous pathogen that causes significant morbidity and mortality. Before the discovery of antibiotics the mortality rate for S. aureus infections approached 90%. As antibiotic resistance spreads and disturbingly aggressive S. aureus strains emerge, there is an urgent need to understand the lifestyle of this wily bacterium in order to develop innovative treatment strategies.

Approximately 30% of healthy individuals are colonized with S. aureus. The ability of S. aureus to inhabit mammals and cause disease is dependent on the coordinated regulation of a diverse array of virulence factors. In many cases, this ultimately results in the colonization of mammalian surfaces and the formation of a bacterial biofilm. The challenge presented by biofilm infections is the remarkable resistance to both host immune responses and available chemotherapies. In response to certain environmental cues, bacteria living in biofilms are capable of using active mechanisms to leave biofilms and return to the planktonic (free-living) state in which sensitivity to antimicrobials is regained. Therefore an improved understanding of the molecular mechanisms of biofilm detachment could facilitate the discovery of innovative treatment options.

Current work is focused on elucidating molecular mechanisms employed by S. aureus to colonize, persist on, and disperse from biologically relevant surfaces. We are also uncovering mammalian host factors and poly-microbial interactions that influence these processes.

Center, Program and Institute Affiliations

Center for Biocatalysis and Bioprocessing

Selected Publications

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Syed A, Ghosh S, Love N, Boles B.  Triclosan Promotes Staphylococcus aureus Nasal Colonization.  MBio.  2014 April 8. 5(2):e01015.
[Link]

Schwartz K, Boles B.  Microbial amyloids--functions and interactions within the host.  Curr Opin Microbiol.  2013 February. 16(1):93-9.
[Link]

Payne D, Martin N, Parzych K, Rickard A, Underwood A, Boles B.  Tannic acid inhibits Staphylococcus aureus surface colonization in an IsaA-dependent manner.  Infect Immun.  2013 February. 81(2):496-504.
[Link]

Boles B, Horswill A.  Swimming cells promote a dynamic environment within biofilms.  Proc Natl Acad Sci USA.  2012 August 7. 109(32):12848-9.
[Link]

Schwartz K, Syed A, Stephenson R, Rickard A, Boles B.  Functional amyloids composed of phenol soluble modulins stabilize Staphylococcus aureus biofilms.  PLoS Pathog.  2012. 8(6):e1002744.
[Link]

Pynnonen M, Stephenson R, Schwartz K, Hernandez M, Boles B.  Hemoglobin promotes Staphylococcus aureus nasal colonization.  PLoS Pathog.  2011 July. 7(7):e1002104.
[Link]

Boles B, Singh P.  Endogenous oxidative stress produces diversity and adaptability in biofilm communities.  Proc Natl Acad Sci USA.  2008 August 26. 105(34):12503-8.
[Link]

Boles B, Horswill A.  Agr-mediated dispersal of Staphylococcus aureus biofilms.  PLoS Pathog.  2008 April 25. 4(4):e1000052.
[Link]

Boles B, Thoendel M, Singh P.  Rhamnolipids mediate detachment of Pseudomonas aeruginosa from biofilms.  Mol Microbiol.  2005 September. 57(5):1210-23.
[Link]

Boles B, Thoendel M, Singh P.  Self-generated diversity produces "insurance effects" in biofilm communities.  Proc Natl Acad Sci USA.  2004 November 23. 101(47):16630-5.
[Link]

Date Last Modified: 11/20/2014 - 14:32:34