The University of Texas Medical School at Houston
Department of Microbiology and Molecular Genetics

Michael C. Lorenz, Ph.D.


  • Associate Professor
  • Department of Microbiology &
    Molecular Genetics
  • University of Texas-Houston Medical School
    6431 Fannin Street, MSB 1.209
    Houston, Texas 77030
  • Telephone: (713) 500-7422
    Laboratory Telephone: (713) 500-7426
  • Lorenz Lab web site


Ph.D., Duke University, 1997

Postdoctoral Fellow, MIT Whitehead Institute

Research Interests:

Understanding the molecular basis of fungal infections

Infectious diseases represent one of the most fascinating, and important, fields of microbiology. The human body is one of the most complex and dynamic environments to which microbes have adapted, and understanding these adaptations is the key to improving treatment. Infections from eukaryotic pathogens, such as fungi, are particularly difficult to treat because of the extensive similarities in cell physiology between fungal and human cells.

My laboratory studies the most important of the fungal pathogens. Candida albicans causes a disseminated bloodstream infection that is fatal in about 40% of cases. For most of us, however, Candida is a normal and harmless part of our microbiota - the community of microorganisms that lives in and on us. The difference between Candida as a deadly pathogen and Candida as a benign commensal is the status of the host's immune system. Infection occurs in people with immunodeficiencies of some kind.

Thus, we are particularly interested in studying the interaction between C. albicans and cells of the immune system, primary phagocytic cells such as macrophages. In vitro, this interaction is extremely dynamic (see figure below). Phagocytosis stimulates a dramatic morphological change, which helps the yeast escape killing by the macrophage. These filaments, or hyphae, are only a small part of this response, however. We have shown that there are equally dramatic changes to cellular physiology and metabolism when C. albicans is confronted with a phagocytic cell. These changes in carbon metabolism, in particular, are critical during infections and we are very interested in the regulatory and signaling networks that control these responses.

Selected Publications:

  • Jiménez-López, Lorenz, M.C. (2013) Fungal immune evasion in a model host-pathogen interaction: Candida albicans versus macrophages. PLoS Pathog. In press.
  • Garsin, D.A., Lorenz, M.C. (2013) Candida albicans and Enterococcus faecalis in the gut: Synergy in commensalism? Gut Microbes 13:409-415. [abstract]
  • Lorenz, M.C. (2013) Carbon catabolite control in Candida: New wrinkles in metabolism. mBio 4:e00034-13. [abstract]
  • Jiménez-López, C., Collette, J.R., Brothers, K.M., Shpardson, K.M., Cramer, R.A., Wheeler, R.T., Lorenz, M.C. (2013) Candida albicans arginine biosynthetic genes in response to host-derived reactive oxygen species. Eukaryot. Cell. 12:91-100. [abstract]
  • Cruz, M.R., Graham, C.E., Gagliano, B.C., Lorenz, M.C.*, Garsin, D.A.* (2013) Enterococcus faecalis inhibits hyphal morphogenesis and virulence of Candida albicans. Infect. Immun. 81:189-200. [abstract]
  • Xu, T., Tripathi, S.K., Feng, Q., Lorenz, M.C., et al. (2012) A potent plant-derived antifungal acetylenic acid mediates its activity by interfering with fatty acid homeostasis. Antimicrob. Agents Chemother. 56:2894-2907. [abstract]
  • Cottier, F., Raymond, M., Kurzai, O., Bolstad, M., Leewattanapasuk, W., Jiménez-López, C., Lorenz, M.C., et al. (2012) The bZIP transcription factor Rca1p is a central regulator of a novel CO2-sensing pathway in yeast. PLoS Pathog. 8:e1002485. [abstract]
  • Collette, J.R., Lorenz, M.C. (2011) Mechanisms of immune evasion in fungal pathogens. Curr. Opin. Microbiol. 14:668-675. [abstract]
  • Vylkova, S., Carman, A.J., Danhof, H.A., Collette, J.R., Zhou, H., Lorenz, M.C. (2011) The fungal pathogen Candida albicans autoinduces hyphal morphogenesis by raising extracellular pH. MBio. 17;2:e00055-11. [abstract]
  • Lorenz, M.C. (2010) Host-microbe interactions: fungi. Curr. Opin. Microbiol. 13:389-391. No abstract available.
  • Butler, G, et. al. (2009) Evolution of pathogenicity and sexual reproduction revealed by comparing eight Candida genomes. Nature 459:657-662. [abstract]
  • Ramírez, M.A., Lorenz, M.C. (2009) The transcription factor homolog CTF1 regulates β-oxidation in Candida albicans. Eukaryot. Cell. 8:1604-1614. [abstract]
  • [Search PubMed for more papers by Michael Lorenz]