Professor of Infection Biology
Laboratory of Infection Biology
Department of Medicine I
Medical University Vienna
Währinger Gürtel 18-20, 1090 Vienna
Phone: +43 (0)1 40400 - 51390
FAX: +43 (0)1 40400 - 51670
Innate Immunity; Immunity to Microbes; Macrophage Polarization and Function, endogenous modulators of inflammation, innate lymphoid cells.
Innate Immunity in Infection and Inflammation
Our research projects are addressing important clinical problems and focusing on innate immune mechanisms with relevant bacterial infections simulated under laboratory conditions. While our general objectives are in furthering our understanding of clinically relevant pathogens and host-pathogen interactions; our primary objectives are to positively impact and substantially enhance the current diagnostic procedures and ultimately influence therapies and survival.
Our main objectives are:
- To understand the regulation of inflammatory responses and receptor crosstalk during clinically relevant bacterial infections and sterile inflammation
- To investigate the biological impact of endogenous modulators of the inflammatory response
- To study the contribution of innate (lymphoid) cells to immune homeostasis and host defense
Pattern recognition receptors (PRR) are critical components of innate immunity that recognize and signal the presence of pathogens. Increasing evidence illustrates that most microbes are simultaneously sensed via the involvement of several classes of PRRs, which interact in a cooperative or complementary fashion. We wish to understand how additional receptors and mediators complement known functions of PRRs in order to provide an optimized immune response to a specific pathogen.
Our secondary focus of interest is on the role and function of endogenous (danger) molecules in the inflammatory response, as we believe that targeting these molecules might allow for immune-modulatory effects that can be used in the clinics.
Recently, we became interested in the maintenance of immune homeostasis of distinct organs, since understanding these homeostatic mechanisms might help us comprehend the organ-specific response to infection and injury – and hence provide therapeutic targets.
We address these questions by simulating infectious and inflammatory diseases under laboratory conditions, and by applying techniques that involve bone marrow chimeras, adoptive transfer experiments, FACS analysis, gene expression analysis, various functional macrophage assays, as well as microscopy and protein based assays.
More information about the various research projects can be found <here>
Warszawska, J. M., R. Gawish, O. Sharif, S. Sigel, B. Doninger, K. Lakovits, I. Mesteri, M. Nairz, L. Boon, A. Spiel, V. Fuhrmann, B. Strobl, M. Muller, P. Schenk, G. Weiss, and S. Knapp. 2013. Lipocalin 2 deactivates macrophages and worsens pneumococcal pneumonia outcomes. J Clin Invest: 3363-3372.
Matt, U., O. Sharif, R. Martins, T. Furtner, L. Langeberg, R. Gawish, I. Elbau, A. Zivkovic, K. Lakovits, O. Oskolkova, B. Doninger, A. Vychytil, T. Perkmann, G. Schabbauer, C. J. Binder, V. N. Bochkov, J. D. Scott, and S. Knapp. 2013. WAVE1 mediates suppression of phagocytosis by phospholipid-derived DAMPs. J Clin Invest 123: 3014-3024.
Sharif, O., U. Matt, S. Saluzzo, K. Lakovits, I. Haslinger, T. Furtner, B. Doninger, and S. Knapp. 2013. The scavenger receptor CD36 downmodulates the early inflammatory response while enhancing bacterial phagocytosis during pneumococcal pneumonia. J Immunol 190: 5640-5648.
Zivkovic, A., O. Sharif, K. Stich, B. Doninger, M. Biaggio, J. Colinge, M. Bilban, I. Mesteri, P. Hazemi, R. Lemmens-Gruber, and S. Knapp. 2011. TLR 2 and CD14 mediate innate immunity and lung inflammation to staphylococcal Panton-Valentine leukocidin in vivo. J Immunol 186: 1608-1617.
Baumann, C. L., I. M. Aspalter, O. Sharif, A. Pichlmair, S. Bluml, F. Grebien, M. Bruckner, P. Pasierbek, K. Aumayr, M. Planyavsky, K. L. Bennett, J. Colinge, S. Knapp*, and G. Superti-Furga*. 2010. CD14 is a coreceptor of Toll-like receptors 7 and 9. J Exp Med 207: 2689-2701.