Insight into inflammatory diseases – understanding the molecular mechanisms during the onset and resolution of inflammation
The immune system is the body's natural defence system that protects against invading germs and prevents disease development. For its optimal function the immune system must recognize a wide variety of damaging agents, such as bacteria, viruses, and parasites but also other harmful substances from the environment. Our immune system is divided into two main subsystems, the innate the adaptive immunity. Throughout the first hours and days of exposure to microbes the innate immunity is the key branch of the immune system that contends against pathogens. It restricts and eliminates infections or other initial causes of cell injury by inducing and resolving inflammation. Tight regulation of the innate immunity is essential to ensure an efficient defence against invading pathogens and to control inflammatory processes. Imbalances in activation or resolution of inflammatory processes might have dramatic outcomes by driving the development of inflammatory and autoimmune diseases but also cancer development. To date, there are no potent therapeutic strategies available to cure these disorders and further research is required to understand innate immune regulatory mechanisms driving disease development.
My research aims to understand the regulation of pattern recognition receptors – a hallmark of the innate immunity. These receptors recognize microbial compounds or molecules that are released from damaged tissue. Receptor activation triggers an induction of inflammatory mediators, which orchestrate the destruction of invasive microbes. Among the key inflammatory processes activated upon infection is the formation of a multi-protein complex called inflammasome. Inflammasomes play a vital role in the secretion of particular inflammatory mediators such as members of the interleucin-1 family that help to recruit immune cells to sites of infection and inflammation. If dysregulated, inflammasomes often contribute to the development of inflammatory diseases such as atherosclerosis and rheumatoid arthritis and reduced pathogen clearance with dramatic outcomes showing the importance of the in-depth analysis of these regulatory mechanisms.
My research group is focusing on the identification of new molecules in innate immunity - in particular inflammasome regulation. Using state-of-the-art tools in cell and molecular biology and genetics we aim to uncover new key players in inflammasome regulation and to identify the underlying molecular mechanisms by which these molecules modulate innate immunity during infection and inflammation. We are interested in gaining knowledge of basic molecular mechanisms that might be dysregulated during disease progression. In addition, by applying different in vivo models of infection and inflammation, our research will extend the present knowledge of the physiological relevance of these newly identified molecules. Together, this will provide new target molecules for therapeutic treatments of infectious and inflammation-driven diseases.
If you are interested in joining the team as an undergraduate student or post-doc, please send me a short letter of motivation and your CV (email: email@example.com).
Group members and contact information
Saskia Erttmann, PhD Assistant Professor e-mail: firstname.lastname@example.org
Preeti Moar, Master of Science Postdoctoral fellow e-mail: email@example.com
Lucas Riedel Project student (Master student from University of Bielefeld)
Former group members
Lucía Pérez Jiménez Bachelor student from Jan. - June 2019
Amanda Pereira de Freitas Postdoctoral fellow from Oct. 2019 - Oct. 2020
Erttmann S.F. and N.O. Gekara. Hydrogen peroxide release by bacteria suppresses inflammasome-dependent innate immunity. Nature Communications. 10 (1), 1-13. 2019.
Erttmann S.F., A. Härtlova, M. Sloniecka, A. Hosseinzadeh, R. Rofougaran, F.A.M. Raffi, U. Resch, T. Edgren, M. Fällman, T. Ek and N.O. Gekara. Loss of the DNA damage repair kinase ATM impairs inflammasome dependent anti-bacterial innate immunity via oxidative stress. Immunity. 45(1):106–118. 2016.
Wang H., K. Avican, A. Fahlgren, S.F. Erttmann, A.M. Nuss, P. Dersch, M. Fällman, T. Edgren and H. Wolf-Watz. Increased plasmid copy-number is essential for Yersinia T3SS function and virulence. Science. 253(6298):492-495. 2016.
Härtlova A., S.F. Erttmann, F.A. Raffi, A.M. Schmalz, U. Resch, S. Anugula, S. Lienenklaus, L. M. Nilsson, A. Kröger, J. A. Nilsson, T: Ek, S. Weiss and N.O. Gekara. 2015. DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity. Immunity. 42(2):332-343. 2015.