Welcome to the Department of MMI

The Department of Molecular Microbiology and Immunology's (MMI) mission is to maintain active and integrated research programs that study the interactions between microbes and their hosts. The goal is to understand how these influence the outcome of infection and disease progression. Current research interests in the department include understanding host signaling in response to viral infection, molecular mechanisms of NK and NK T cell activation, and molecular principles underlying fungal pathogenesis. This work provides an interdisciplinary structure for our training programs.

MMI supports undergraduate, graduate, and postdoctoral education in the areas of microbiology and immunology. Departmental instruction includes lecture courses, seminar courses, and laboratory research (both undergraduate independent study and graduate thesis). We foster collaborative studies within the department as well as with faculty in other departments, both on campus and hospital-based.

MMI News 

Antifungal tolerance is a subpopulation effect distinct from resistance and is associated with persistent candidemia
Population heterogeneity is an important strategy that pathogens can utilize to escape antimicrobial treatment. This is now evidenced by our work in Candida albicans, a prevalent fungal pathogen that can occupy diverse niches in the human body, either as a commensal or as an invasive pathogen. Antifungal resistance has been described for all drugs used to treat infections by this species. Frontline therapies include azoles, a class of drugs which target the fungal cell membrane and inhibit cell growth.  We now show that population heterogeneity of infecting isolates can enable azole escape – in many strains a subpopulation of C. albicans cells can still grow, albeit slowly, in the presence of high drug concentrations.


Surviving Deadly Lung Infections: Innate Host Tolerance Mechanisms in the Pulmonary System
Much research on infectious diseases focuses on clearing the pathogen through the use of antimicrobial drugs, the immune response, or a combination of both. Another way to survive an infection is to tolerate the alterations to homeostasis that occur during a disease state through a process called host tolerance or resilience, which is independent from pathogen burden. Alterations in homeostasis during infection are numerous and include tissue damage, increased inflammation, metabolic changes, temperature changes, and changes in respiration. By understanding tolerance mechanisms in the lung we can better address treatment options for deadly pulmonary infections.


Congratulations to Jenna Wurster who has received an NSF Fellowship Award for her work in the Belenky Lab!



Congratulations to Benjamin Korry who has received an NSF Fellowship Award for his work in the Belenky Lab!


Microbial competition between Escherichia coli and Candida albicans reveals a soluble fungicidal factor
Localized and systemic fungal infections caused by Candida albicans can lead to significant mortality and morbidity. However, severe C. albicans infections are relatively rare, occurring mostly in the very young, the very old, and immunocompromised individuals. The fact that these infections are rare is interesting because as much as 80 percent of the population is asymptomatically colonized with C. albicans. It is thought that members of the human microbiota and the immune system work in concert to reduce C. albicans overgrowth through competition and modification of the growth environment. Here, we report that Escherichia coli (strain MG1655) outcompetes and kills C. albicans (strain SC5314) in vitro. We find that E. coli produces a soluble factor that kills C. albicans in a magnesium-dependent fashion such that depletion of available magnesium is essential for toxicity.


Epigenetic control of pheromone MAPK signaling determines sexual fecundity in Candida albicans

A central theme in biology is to understand how different signaling outputs can be accomplished by changes to signal transduction pathways. Here, we examined epigenetic differences between two cell states in the human fungal pathogen Candida albicans. We show that cells in the “white” state are sterile due to multiple bottlenecks in MAPK signaling relative to mating-competent “opaque” cells. Alleviation of these bottlenecks by reverse engineering effectively converts sterile white cells into sexually competent cells. These results have broad implications for understanding how epigenetic changes can impact MAPK expression and signaling output, including events associated with tumorigenesis. We also propose a model for how the white-opaque switch gained control of sexual reproduction in Candida during evolution.

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