LieszLab - Stroke-Immunology
We are interested in the interplay between the brain and the immune system after stroke. Acute brain lesions disturb the well-balanced interconnection between both systems. Hence, our research focuses on both directions of brain-immune interaction: The impact of immune mechanisms on neuronal damage and recovery and the systemic immunomodulation after stroke.
Our methodological spectrum covers diverse brain ischemia models, transgenic animal models, a broad spectrum of cutting-edge immunological techniques as well as histological, biomolecular and behavioral analysis tools.
The lab has a strong translational research focus with the ultimate goal to develop novel diagnostic tools, therapies and mechanistic insights on the highly complex disease which stroke represents. In order to achieve this, a premise of our work is to address key unmet needs of stroke patients and make use of translationally relevant tools.
Currently, the laboratory focuses on three main research topics within the area of brain-immune interaction:
A focus of our work is the role of pro- and anti-inflammatory lymphocyte subpopulations in stroke and their neurotoxic and – protective functions. Following our previous work in this field (e.g. Nature Medicine, 2009, The Journal of Neuroscience, 2013) we have recently characterized a key role of the intestinal microbiome in modulating lymphocyte function after stroke (The Journal of Neuroscience, 2016 and Brain Behav Immun 2017). We are investigating the impact of bacterial mediators and mechanisms of microbiota-immune communication after stroke.
Another focus of our research is the migration of pro-inflammatory leukocytes to the ischemic brain (Brain, 2011). We are investigating pathophysiological mechanisms of leukocyte-endothelial interaction and novel therapeutic approaches for translational use (Science Translational Medicine, 2015). We have recently identified the choroid plexus as a previously unrecognized invasion pathways (Acta Neuropathologica, 2017) and are further striving to understand the differential role of alternative invasion routes to the injured brain.An alarmin(g) consequence of stroke: Brain-released alarmins and sterile inflammation
A third research area investigates alarmin-driven mechanisms of peripheral immune alterations after brain ischemia. We aim to characterize alarmins—humoral mediators released by the necrotic brain tissue—as modulators of the systemic immune system (The Journal of Neuroscience, 2015). We recently described alarmins as key mediators leading to the exacerbation of vascular inflammation and atherosclerosis after stroke (Science Translational Medicine, 2018).
Contact: Arthur Liesz