Ph.D. from the Friedrich Schiller University Jena, Germany (2005 - 2010)

• Research performed at the Leibniz Institute for Natural Product Research and Infection Biology
• Mentor: Axel A. Brakhage

Visiting Scientist at LABiomed, Harbor UCLA, Los Angeles (2008)

• Mentor: Scott G. Filler

Postdoc at the University of California, Irvine (2010 - 2016)

• Mentor: Manuela Raffatellu

Things you cannot see with the naked eye - they have always fascinated me. The first victims for my microscope were plants, but very quickly I discovered my love for less stationary - but my no means less complex - research subjects: Microbes.

My first research projects involved an opportunistic human pathogenic fungus: Aspergillus fumigatus. While you can certainly see it with the naked eye (envision mold on your bread), it fit my research interests perfectly. What happens on the molecular level and during pathogenesis of this fungus was truly fascinating.

Aspergillus fumigatus is spread via spores, which are inhaled and can reach the alveoli of the lungs. My research at the Leibniz Institute for Natural Product Research and Infection Biology in Germany uncovered that spores bind complement regulatory molecules of the human host. With these regulators bound to the surface, spores downregulate the activation of the host complement cascade (PMC2223477). In an immunocompromised host (e.g. due to chemotherapy), these spores can germinate and elongate into hyphae. These hyphae are, contrary to spores, metabolically active and secrete proteases. One of these proteases cleaves complement components and thereby downregulates complement activation PMC2916278.

The fungus Aspergillus is fascinating and complex, but one thing it is not: a true pathogen. In order to study the interaction of a true pathogen with the host, I switched my attention to Salmonella enterica serovar Typhimurium. This bacterium causes inflammatory diarrhea in healthy people, and disseminates to peripheral organs in immunocompromised patients. At the University of California, Irvine, I studied the role of cytokine IL-22, which is highly upregulated during the infection with Salmonella. My research showed that this host protein has an unusual function: it promotes the growth of Salmonella in the gut lumen. IL-22 induces the production of antimicrobial proteins, but instead of killing Salmonella, these antimicrobial proteins help Salmonella outcompete the resident microbes in the gut. Antimicrobial proteins kill resident microbes, but Salmonella is resistant and grows to high numbers in the gut (PMC3964146).

Currently, I am combining my experience with fungi and Salmonella. In my lab we are studying the role of resident (commensal) fungi in the gut during Salmonella infection.