Servizio Comunitario di Informazione in materia di Ricerca e Sviluppo - CORDIS

Periodic Report Summary 1 - NEUROINFLAMMATION (nEUROinflammation)

In Europe about 650,000 patients die from strokes each year and a similar number suffers from multiple sclerosis. Both disorders have a marked neuroinflammatory response in common, while the relative importance of the innate and adaptive immunity seems to differ. The two arms of the immune system are linked by myeloid cells, i.e. resident microglia and invading bone marrow-derived macrophages. Intriguingly, myeloid cells exert both detrimental and beneficial effects in the brain, while the underlying mechanisms are largely unclear. The Marie Curie Initial Training Network (ITN) nEUROinflammation funded by the European Commission Seventh Framework Programme (FP7) for Research and Technological Development (2007-2013) searches for strategies to modulate myeloid cell behaviour in the brain for therapeutic purposes. This study includes the blood-brain barrier as the gate-keeper that controls the invasion of myeloid cells. A unique feature of this ITN is to combine stroke and multiple sclerosis research in order to release synergies between the fields and to provide a comprehensive picture of neuroinflammation. This ITN aims at one goal: to modulate basic neuroinflammatory mechanisms for the treatment of neurological diseases.
In nEUROinflammation sixteen partners from the academic and private sector with complementary scientific background have joined forces. Partners have expertise in various models of stroke and multiple sclerosis. Furthermore, they have acquired a large toolbox of methods to characterize neuroinflammation in an experimental and clinical setting. By employing a range of experimental and translational techniques partners train 13 Early Stage Researcher (ESRs) in neuroinflammatory concepts and technologies that are valid across specific disease entities. Work is structured according to key cellular players of neuroinflammation, i.e., bone marrow-derived macrophages (WP1), endothelial cells (WP2), and resident microglia (WP3). In two very fruitful scientific meetings in Caen and Brescia, both in 2014, and a summer school in Lübeck 2015 we have reinforced our close collaborations and coordinated the next steps to approach our research questions.
Starting on October 1st 2013, nEUROinflammation runs for four years. After the first 24 months of our project, preliminary results have been obtained. In WP1 “Bone-marrow derived macrophages and dendritic cells in neuroinflammation” Marta Jordao (ESR1), Freiburg, Germany, has established the tools to investigate the turnover rates of bone marrow-derived macrophages and their role in activating T cells in experimental autoimmune encephalomyelitis. Mattia Gallizioli (ESR2), Barcelona, Spain, has obtained the first results on the effect of dendritic cell expansion on stroke outcome. In this context, Rittika Chunder (ESR3), Lübeck, Germany, is analyzing autoantibodies in human stroke patients in close cooperation with partner 2 in Barcelona, Spain. Meike Keuters (ESR4), Kuopio, Finland, is in the process of characterizing the role of immunomodulatory and mast cell targeting drugs in models of inflammation and stroke.
In WP2 “Pivotal role of endothelium in mediating neuroinflammation” Pascale Baden (ESR5), Bern, Switzerland, studied the function of claudin 3 for the blood-brain barrier and the development of experimental autoimmune encephalomyelitis using knockout mice. Omar Chuquisana (ESR6), Münster, Germany, is investigating the role of β2 integrin for the adhesion of neutrophils to endothelial cells in ischemic stroke. Focusing on the barrier properties of endothelial cells Claudio Derada Troletti (ESR7), Amsterdam, Netherlands, investigates the role of miRNAs during inflammation. The work of Anupriya Mehra (ESR8), Caen, France, is centering on the role of NMDA receptors in brain endothelial cells and tries to target these receptors to ameliorate neuroinflammation. Finally, Yun Jiang (ESR9), Lübeck, Germany, is probing the role of the pro-inflammatory NF-κB signaling pathway for small vessel diseases and the development of spontaneous cerebral ischemia.
In WP3 “Protective and detrimental role of microglia” Wenson D. R. Karunakaran (ESR10), Warsaw, Poland, is characterizing microglial gene expression in in-vitro and in-vivo models of glioma and stroke. He is focusing on epigenetic regulation of microglial gene expression together with Mariana Mota (ESR11), Brescia, Italy, who attempts to modulate epigenetic control by using pharmacological tools. Nozha Borjini (ESR12), Parma and Bologna, Italy, is in the process of performing a time course analysis of potential biomarkers for inflammation and demyelination in an experimental autoimmune encephalomyelitis model searching for early markers that predict clinical outcome. Finally, Natalia Kolosowska (ESR13), Kuopio, Finland, is exploring the role of exosomal miRNA in the neuroprotection exerted by inflammatory stimuli in a mouse model of stroke.
Continuing along these lines, we expect results of the consortium in two areas. First the consortium has the chance to refine current concepts on how myeloid cells invade the brain in two common neurological diseases and how they shape brain injury. While this may not lead to immediate improvements in health care, it provides a rational and sound basis for further drug development. Up to now the scientific merits of the consortium are documented by 12 publications - and counting. Second and equally important, the consortium takes pride in training 13 talented ESRs that will contribute to the European scientific community and to the future investigation of neuroinflammatory diseases.
For further information please visit the nEUROinflammation website: or contact the coordinator Markus Schwaninger, University of Lübeck, Institute of Pharmacology and Toxicology, Ratzeburger Allee 160, 23538 Lübeck, Germany, Tel.: +49-451-500 2680, E-Mail:

Reported by



Life Sciences