Karl Kuchler has a long-standing interest in fungal infection biology, molecular genetics, as well as host immune signaling at their intersections with the molecular mechanisms of antifungal drug resistance. His work discovered a novel TLR7-dependent fungal response pathway in dendritic cells, and the group discovered a molecular mechanism underlying the hyper-inflammatory host response upon fungal infections. Finally, the most work uncovered pivotal roles of fungal HDACs/HATs in controlling antifungal drug resistance, stress response, DNA repair as well as virulence.
Research
Karl Kuchler is interested in studying fundamental problems in infection biology using a combination of molecular as well as genome-wide and systems biology approaches. We are particularly interested in a better understanding of the dynamic gene regulation during host-pathogen interplay, with a focus on fungal pathogens such as Candida spp.
On the pathogen side, we use reverse genetics, systems biology and functional genomics strategies (gene deletions, RNA-Seq / Chip-Seq) to identify virulence and antifungal drug resistance genes, decipher the role of histone modifications and chromatin alterations in morphogenetic switching or cell fate determination, and study signaling mechanisms during fungal morphogenesis and host colonization.
On the host side, we exploit transcriptomics and proteomics of primary phagocytes (macrophages, dendritic cells, neutrophils) and T cells to study the mechanisms of gene regulation underlying fungal immunity, The interplay of adaptive (T cells) and innate (dendritic cells) immunity in fungal surveillance, and type I interferon signaling (i.e. IFNbeta) and inflammation controlling the function and activity of inflammatory phagocytes (monocytes, neutrophils and T cells), and the critical role of Th17 inflammation on pathogen elimination in invasive fungal diseases
For more information please visit http://www.cdl.univie.ac.at/