Michael D. Kruppa  

Michael Kruppa, PhD
Assistant Professor, Department of Biomedical Sciences

Contact Information:

Carl A Jones Hall (VA Bldg 1) Room 1-33
Phone: 423-439-6248


1988-1992       B.S. St. Mary’s University, San Antonio, Texas, Department of Biology  

1994-2000       Ph.D. University of Texas Health Science Center at San Antonio, Department of  Microbiology & Immunology

2000-2005       Postdoctoral Fellow, Georgetown University Medical School (GUMC) Department of Microbiology & Immunology.

2005-2007       Research Assistant Professor (GUMC)

2008- Present  Assistant Professor in the Department of Microbiology (Biomedical Sciences since 2012) at ETSU

  Research interests:

My Laboratory has several ongoing research projects. My primary research interest is understanding the mechanism of how the opportunistic fungus Candida albicans regulates its ability to undergo morphogenesis through a process called quorum sensing.  Quorum sensing in C. albicans is due to the expression of a molecule called farnesol.  As farnesol is expressed, the increasing concentration of the molecule inhibits the ability of the organism to undergo morphogenic shift from a yeast growth form to that of a hyphal growth form.  The ability to sense farnesol and control morphogenesis contributes to the ability of C. albicans to be virulent in a host organism.  Ultimately our goal is to understand how this process works and to develop new molecules that target the quorum sensing regulatory pathway(s) as possible new antifungal compounds.

A second project that is an off-shoot from C. albicans quorum sensing, is investigating how the fungus interacts with other microbial species as a reflection of interspecies communication relating to control of C. albicans morphogenesis.  We are interested in understanding the interspecies interactions that take place in clinically important niches, both in the host and on abiotic surfaces in the form of biofilms. Biofilms are a major source for hospital acquired infections and are rather resistant to antimicrobials, and understanding how the microbial communities that make up these biofilms communicate and compete for space may help give clues as to how microbes can persist and survive antibiotic treatment.

Interaction with C. albicans. .

Figure 1. Interaction with C. albicans. On the left shows a mutant colony that shows normal inhibition of filamentation on an agar surface when grown in the presence of bacteria under filament inducing conditions. On the right, a mutant strain that can filament in the presence of the same bacteria suggesting that this mutant cannot recognize a communication signal released from the bacteria .

A third project, in collaboration with Dr. David Williams (Surgery-ETSU) is on the role of glucans and how they are recognized by the host. Glucans from several fungal sources are being purified and characterized for their structure and used with in vitro and in vivo models to understand host recognition and response to fungal carbohydrates.

Selected Publications:

Kruppa, M ., T. Goins, J.E. Cutler, D.W. Lowman, D. Williams, N. Chauhan, V. Menon, P. Singh and R. Calderone. 2003.The role of the Candida albicans histidine kinase (CHK1) in the regulation of cell wall mannan and glucan biosynthesis. FEMS Yeast Res. 3: 289-299. 

Kruppa, M . and R. Calderone. 2006. Two-component signal transduction in the human fungal pathogens. FEMS Yeast Res. 6(2):149-59. 

Chauhan, N., M. Kruppa , and R. Calderone. 2007. The Ssk1p response regulator and Chk1p histidine kinase mutants of Candida albicans are hypersensitive to fluconazole and voriconazole. AAC. 51:3747-51. 

Kruppa, M. 2009. Quorum Sensing and Candida albicans Mycoses. 52:1-10. 

Li, D., Williams, D., Lowman, D., Monteiro, M.A., Tan, X., Kruppa, M., Fonzi, W., Roman, E., Pla, J., and R.Calderone. 2009. The Candida albicans histidine kinase Chk1p: Signaling and cell wall mannan. Fungal Gen Biol. 731-741.  

Bambach, A., Fernandes, M., Ghosh, A., Kruppa, M ., Alex, D., Li, D., Fonzi, W., Chauhan, N., Sun, N., Agrellos, O., Vercesi, A., Rolfes, R.J., and R. Calderone. 2009. The Goa1p of Candida albicans localizes to the mitochondria during stress and is required for mitochondrial function and virulence. Eukary Cell. 1706-1720.

Kruppa, M.D., Lowman, D., Chen,Y-H., Selander, C., Scheynius, A., Monteiro, M.A., and D. L. Williams. Identification of (1→6)-β-D-glucan as the major carbohydrate component of the Malassezia sympodialis cell wall. Carbohydr Res.2474-2479.  

M. Kruppa , R. R. Greene, I. Noss, D. W. Lowman and D. L. Williams. C. albicans increases cell wall mannoprotein, but not mannan, in response to blood, serum and cultivation at physiological temperature. Glycobiology, 21:1173-80. 

D. W. Lowman, H. E. Ensley, R. R. Greene, K. J. Knagge, D. L. Williams and M. D. Kruppa. Mannan structural complexity is decreased when Candida albicans is cultivated in blood or serum at physiological temperature. Carbohydrate Res. 346 (2011) 2752–2759 

D. W. Lowman, L. J. West, D. W. Bearden, M. F. Wempe, T.D. Power, H. E. Ensley, K. Haynes, D. L. Williams.1, and M. D. Kruppa . Characterization of (1g3,1g6)-β-D-Glucan Side Chain Structure Provides the Basis for a New Model of Fungal Cell Wall Rigidity and Flexibility. Plos One. 6(11): e27614. doi:10.1371/journal.pone.0027614