Michael Kruppa, PhD
Associate Professor, Department of Biomedical Sciences
Carl A Jones Hall (VA Bldg 1) Room 133
Lab: Bldg 119, Rm 312,313
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
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.
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.