Biography

Dr. Lorenz joined the faculty of the Department of Microbiology and Molecular Genetics at McGovern Medical School in 2003 as an Assistant Professor.  In 2023 he was named chair of MMG and is proud to be part of this dynamic community dedicated to student training and research excellence.

A native of Atlanta, Dr. Lorenz began his research career in infectious disease studying malaria and HIV at the Centers for Disease Control and Prevention.  He earned a B.A. in Biochemistry and Cell Biology at Rice University, where he studied enzyme kinetics with Dr. Fred Rudolph.  Subsequently he was a Ph.D. student in the Department of Genetics at Duke University Medical School, unraveling signaling pathways that regulate cellular differentiation in the model yeast Saccharomyces cerevisiae with Dr. Joseph Heitman.

Dr. Lorenz returned to infectious disease research as a post-doctoral fellow at the Whitehead Institute for Biomedical Research in Cambridge, MA, under the guidance of Dr. Gerald Fink.  It was here that he began his investigations into the mechanisms of pathogenesis in Candida species, one of the most common and deadly fungal causes of invasive disease.

In addition to his current role as Chair of MMG, Dr. Lorenz has served as President of the Medical Mycological Society of the Americas, Chair of Division F (Fungi) of the American Society for Microbiology, and a member of the ASM’s Council on Microbial Sciences.  He has served on numerous grant review panels for the National Institutes of Health and other national and international funding bodies and as an editor for several journals.  He is an elected fellow of the American Academy of Microbiology and the American Association for the Advancement of Science.

Education

B.A.
Rice University, 1992
Ph.D.
Duke University, 1997
Post-doctoral Fellow
Whitehead Institute for Biomedical Research, 2003

Areas of Interest

Research Interests

Understanding the molecular basis of fungal infections

The last few years have emphatically reminded us of the immense toll of infectious diseases on human health remains immense.  This toll is persistent and emerging drug resistance puts us at risk of backsliding on a century of progress in treating these diseases. Fungi are often overlooked as infectious agents, despite causing a spectrum of diseases ranging from mild and common to life-threatening infections responsible for over one million deaths per year. Candida species are particularly problematic, capable of infecting virtually any body site, including the mouth and throat (oral thrush) and the genital tract (vaginal yeast infections), but our primary interest is in the life threatening infections that occur mostly in hospitalized patients with weakened immune systems.  Our tools for managing these infections are inadequate, partly as a result of the cell biological similarities between fungi and humans that make antifungal drug discovery challenging.

 

There are several areas of ongoing research in the Lorenz Laboratory.

 

  • Patients who are at high risk for invasive candidiasis usually have weakened innate immune systems, which includes professional phagocytes like macrophages and neutrophils. The interaction of the most common Candida species, C. albicans, with macrophages is dynamic and dramatic. The immune cell supposed to protect us from microbial pathogen is itself the victim of a remarkable morphological shift in the fungal cell, which forms a filamentous form that pierces the macrophage and destroys it.  We have a long-standing interest in understanding the mechanisms that underlie this aspect of fungal virulence.

 

  • In its normal niche in the human gastrointestinal tract, C. albicans is surrounded by hundreds of bacterial species. In collaboration with MMG faculty member Danielle Garsin, we have identified that one of these, the Gram-positive bacterium Enterococcus faecalis, itself an opportunistic pathogen, produces a small protein that restricts C. albicans to a non-pathogenic state. We have confined the activity of this protein to a short peptide and have shown that it protects animals against several manifestations of candidiasis.  We continue to develop this potential antifungal agent.

 

  • Candida auris is a very concerning emerging pathogen, recognized only a few years ago, that is inherently resistant to some or all current antifungal drugs and is easily transmitted person-to-person in health care facilities. We are investigating the mechanisms of virulence and drug resistance in this new pathogen using transcriptomic and genetic tools.

 

  • C. albicans is a common cause of urinary tract infections and little is known about the host-pathogen biology that contributes to these infections, which commonly manifest as polymicrobial biofilms on within the urinary tract, especially on catheters. In collaboration with MMG faculty member Jennifer Walker, we are studying the transcriptional regulation of biofilm formation in this environment and how we might better manage these infections.

Publications

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Selected recent publications

Vylkova, S. and Lorenz, M.C. (2014) Modulation of phagosomal pH by Candida albicans promotes hyphal morphogenesis and requires Stp2p, a regulator of amino acid transport.  PLoS Pathog. 10:e1003995.  PMID: 24626429.

 

Priest, S.P. and Lorenz, M.C. (2015).  Characterization of virulence-related phenotypes in Candida species of the CUG clade.  Eukaryot. Cell. 14:931-40.  PMID: 26150417.

 

Danhof, H.A.*, Vylkova, S.*, Vesely, E., Ford, A.E., and Lorenz, M.C. (2016)  Robust environmental alkalinization by Candida albicans during growth on dicarboxylic acids.  mBio 7:e01646-16.  PMID: 27935835.

 

Graham, C.E., Cruz, M.R., Garsin, D.A., and Lorenz, M.C. (2017)  The Enterococcus faecalis bacteriocin EntV inhibits hyphal morphogenesis, biofilm formation, and virulence of Candida albicans.  Proc. Nat. Acad. Sci. USA 114:4507-12.  PMID: 28396417.

 

Williams, R.B. and Lorenz, M.C. (2020).  Multiple alternative carbon pathways combine to promote Candida albicans stress resistance, immune interactions and virulence.  mBio 11:e03070-19. PMID: 31937647.

 

Pountain, A.W., Collette, J.R., Farrell, W.M., and Lorenz, M.C. (2021) Interactions of both pathogenic and non-pathogenic CUG clade Candida species with macrophages share a conserved transcriptional landscape.  mBio 12:e03317-21.  PMID: 34903044.

 

Cruz, M., Cristy, S., Guha, S., Buda de Cesare, G., Evdokimova, E., Sanchez, H., Borek, D., Miramon, P., Yano, J., Fidel, P.L., Savchencko, A., Andes, D.A., Stogios, P.J., Lorenz, M.C.*, Garsin, D.A.* (2022) Structural and functional analysis of EntV reveals a 12 amino acid fragment protective against fungal infections. Nat. Comm. 13:6047. PMID: 36229448.

 

Wilson, H.B. and Lorenz, M.C. (2023) Candida albicans hyphal morphogenesis within macrophages does not require carbon dioxide or pH sensing pathways.  Infect Immun. 91:e0008723.  PMID: 37078861.

 

Miramon, P., Pountain, A.W., Lorenz, M.C. (2023) Candida auris-macrophage cellular interactions and transcriptional response.  Infect. Immun. 91:e0027423.  PMID: 37815367.

 

Guha, S., Christy, S.A., Buda de Cesare, G., Cruz, M.R., Lorenz, M.C., and Garsin, D.A. (2024) Optimization of the antifungal properties of EntV by variant analysis.  mBio 9:e0057024.  PMID: 38587425.