• Assistant Professor
• Campus Address: MS 420
• Telephone (317) 274-8143
• E-mail mebauer@iupui.edu
• Lab Website  http://www.iupui.edu/~bauerlab/

 Training

• A.B., 1985:  Washington University
• M.A., 1988:  University of Missouri-Columbia
• Ph.D., 1996:  University of Wisconsin-Madison
• Postdoctoral, 1996-2000:  Indiana University School of Medicine
• Assistant Scientist, 2000-2004:  Indiana University School of Medicine, Department of Medicine, Division of Infectious Diseases

Summary of the focus of the research of Dr. Bauer

Our laboratory focuses on the pathogenesis of bacterial sexually transmitted diseases, with an emphasis on the host-pathogen interactions between Haemophilus ducreyi, which causes chancroid, and the human host. 

Description and summary of your laboratory's research focus

Our research focuses on host-pathogen interactions of the sexually transmitted bacterial pathogen Haemophilus ducreyi.  H. ducreyi is a pathogen of human skin and causes chancroid, a genital ulcer disease endemic in sub-Saharan Africa and Southeast Asia that facilitates the transmission of HIV.  In our research, we use molecular tools and confocal microscopy-based imaging analysis to understand virulence mechanisms by which H. ducreyi survives in vivo.  We identify putative virulence factors and determine their roles in human disease through use of a human model of experimental infection.  We also characterize these virulence factors at the molecular level and develop appropriate functional assays to define their roles in mechanisms such as adherence or resistance to the killing effects of human phagocytes.  We have previously demonstrated that, throughout the course of disease, H. ducreyi survives extracellularly in a milieu of professional phagocytes.  As an extracellular pathogen, H. ducreyi encounters multiple killing mechanisms of the innate immune system.  One such mechanism is production of cationic antimicrobial peptides, which are secreted into the extracellular milieu by resident keratinocytes and infiltrating phagocytes.  We have identified a number of human antimicrobial peptides that cannot kill H. ducreyi; the mechanisms of resistance to these peptides and the contribution of these mechanisms to virulence of the organism are being investigated.  Throughout infection in humans, H. ducreyi is typically surrounded by fibrin in vivo, and several other extracellular pathogens utilize fibrin to evade opsonization or phagocytosis.  Thus, we are currently investigating the interactions between H. ducreyi and fibrin as a protective mechanism during pathogenesis.  Another focus of the lab is to define additional virulence factors based on our recently completed studies that defined a profile of H. ducreyi genes expressed during human infection. 

Publications

Bauer, M. E., K. R. Fortney, A. Harrison, D. M. Janowicz, R. S. Munson, Jr., and S. M. Spinola.  2008.  Identification of Haemophilus ducreyi genes expressed during human infection.  Microbiol. 154:1152-1160. 

Mount, K. L. B., C. A. Townsend, and M. E. Bauer.  2007.  Haemophilus ducreyi is resistant to human antimicrobial peptides.  Antimicrob. Agents Chemother. 51:3391-3393. 

Bauer, M. E., C. A. Townsend, A. R. Ronald, and S. M. Spinola.  2006.  Localization of Haemophilus ducreyi in naturally acquired chancroid ulcers. Microb. Infect. 8:2465-2468. 

Spinola, S. M., C. T. H. Bong, A. Faber, K. R. Fortney, S. Bennett, C. Townsend, B. Zwickl, S. D. Billings, T. L. Humphreys, M. E. Bauer, and B. P. Katz.  2003.  Host effect on outcome in the human challenge model of Haemophilus ducreyi infection.  Infect. Immun. 71:6658-6663. 

Spinola, S. M., M. E. Bauer, and R. S. Munson, Jr.  2002.  Immunopathogenesis of Haemophilus ducreyi infection (chancroid).  Infect. Immun. 70:1667-1676. 

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