- Andreas Bergthaler Group
- Christoph Binder Group
- Christoph Bock Group
- Sylvia Knapp Group
- Robert Kralovics Group
- Stefan Kubicek Group
- Joanna I. Loizou Group
- Jörg Menche Group
- Giulio Superti-Furga Group
- Georg Winter Group
- Chemical Screening, Proteomics and Metabolomics Facility
- Biomedical Sequencing Facility (BSF)
- Keiryn Bennett (Senior Researcher on Leave)
CeMM Director of Medical Affairs
Department of Medicine I, Laboratory of Infection Biology, Medical University Vienna
The Innate Immune Response to Bacterial Infections
Sylvia Knapp’s research concentrates on the innate immune response to bacterial infections in general, focusing specifically on the comprehensive repertoire of macrophage functions in health, development and disease. Her investigations concentrate on the initiation and resolution of clinically relevant infections and on the role of endogenous danger molecules and their interactions with host structures and pathways. Her latest research is directed towards the interplay of immune cells in regulating tissue homeostasis in health and disease.
Innate immunity is the evolutionary conserved arm of the immune system and instrumental in maintaining tissue homeostasis while at the same time providing the tools to immediately sense and respond to danger such as invading pathogens, metabolic stress or injuries. This wide and diverse range of tasks requires an incredible plasticity and flexibility of the players involved, with tissue resident macrophages being essential in orchestrating many of these responses.
Using clinically relevant infection, injury and metabolic stress models, research in the Knapp-Lab is focusing on how host factors can influence the balance of innate responses in steady state and upon danger.
Dysregulation in the balance of innate immune mechanisms can profoundly alter the susceptibility to bacterial and viral infections, and predisposes to chronic diseases. A prime example of dysregulated immune homeostasis occurs following viral lung infections or acute lung injury, which are the medically most important risk factors for secondary bacterial pneumonia. We focus on how host factors impact on pulmonary immune homeostasis in an attempt to identify immune-modulatory mechanisms that can be used to maintain tissue homeostasis and thus prevent secondary infections.
Using systems approaches, the Knapp-Lab aims to unravel temporal response patterns in a given tissue upon infection, to understand the long-term effects of disrupted homeostasis herein. In a second line of research we investigate how perturbed homeostasis in the course of inflammatory or inherited disorders affects the functionality of immune effector cells, thusly affecting outcome from common infectious diseases such as Gram-negative sepsis or pneumococcal pneumonia.
A central question addressed by the Knapp-Lab pertains to the huge functional repertoire of tissue resident macrophages. As such we study how alveolar macrophages, the tissue resident macrophage subset in lungs, exert their pleiotropic functions upon danger and the forces that maintain these cells in a de-activated phenotype at homeostasis. We have identified several players that importantly shape alveolar macrophage functionality and demonstrated their relevance in pneumonia models.
Sylvia Knapp studied Medicine in Vienna and Berlin, is a board-certified Internist and obtained her PhD at the University of Amsterdam. In 2006 she joined CeMM as a Principal Investigator and until recently, she continued her clinical duties while also running her own lab. In 2012 she was appointed Professor of Infection Biology at the Medical University Vienna and in 2015 she became the Director of Medical Affairs at CeMM. She is a member of the Academia.Net circle of excellent female scientists, corresponding member of the Austrian Academy of Sciences and board member of several national and international reviewing and advisory panels.
Orcid ID: orcid.org/0000-0001-9016-5244 (link)
Saluzzo S., et al. First-Breath-Induced Type 2 Pathways Shape the Lung Immune Environment. Cell Rep. 2017 Feb 21; 18(8): 1893–1905. doi:/10.1016/j.celrep.2017.01.071. (abstract)
Martins R, et al. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nat Immunology 2016 Oct 31. doi: 10.1038/ni.3590. (abstract)
Maier BB, et al. Type I interferon promotes alveolar epithelial type II cell survival during pulmonary Streptococcus pneumoniae infection and sterile lung injury in mice. Eur J Immunol. 2016; 46:2175-86. doi: 10.1002/eji.201546201. (abstract)
Castilia V, et al. Type I interferon signaling prevents IL-1β-driven lethal systemic hyperinflammation during invasive bacterial infection of soft tissue. Cell Host Microbe. 2016; 19:375-87. (abstract)
Sharif O, et al. Trem 2 inhibits complement component 1q effector mechanisms and exerts detrimental effects during pneumococcal pneumonia. PLoS Pathog 2014; 10:e1004167. (abstract)
Matt U, et al. WAVE-1 mediates suppression of phagocytosis by phospholipid-derived DAMPs. J Clin Invest 2013; 123:3014-24. (abstract)
Warszwaska JW, et al. Lipocalin-2 deactivates macrophages and worsens pneumococcal pneumonia outcomes. J Clin Invest 2013; 123:3363–72. (abstract)
Baumann CL, et al. CD14 is a co-receptor of Toll-like receptors 7 and 9. J Exp Med 2010; 207:2689-2701. (abstract)