Scientists led by Professor Dr. Ralf Stumm from the University Hospital in Jena, Professor Dr. Elvira Mass from the University of Bonn and Professor Dr. Frederic Geismann from the Memorial Sloan Ketterin Cancer Center in New York have found out in animal experiments on mice that after a stroke, giant eating cells, so-called macrophages, are produced from bone marrow stem cells, migrate into the brain of the affected mice and attack dead and adjacent brain tissue. They also found that such macrophages also exist in the brain and are part of the body’s immune defence. The giant scavenger cells located there are called microglia. If various diseases, including stroke, cause inflammatory processes in the brain, only the macrophages formed in the bone marrow play a role. The question the researchers have asked themselves is whether it makes a difference whether macrophages migrate into the brain or are already resident there. To answer this question, they developed a new method that, by activating a specific gene function (Cxcr4 gene), leads to the generation of coloured fluorescent stem cells from the bone marrow, which then spread through the blood as circulating immune cells. A protein in the bone marrow stem cells causes the macrophages to glow and become visible. However, they made the discovery that the glowing giant scavenger cells from healthy tissue in the brain disappear after only a few days. If, on the other hand, the researchers inactivate gene function, fewer macrophages are attracted into the brain after the stroke, but even then the macrophages do not completely retreat into the dead tissue and remain in parts of the healthy tissue. The inactive function also leads to the absence of a protective immune response and resident macrophages tend to form inflammation-promoting genes. Therefore, if the mice lack the Cxcr4 receptor, which assumes a protective effect, this leads to greater tissue damage in the brain and consequently to a poorer state of health of the animals. The receptor is therefore part of an immune response and if this is missing, the protective effect of the bone marrow-derived macrophages does not take place in the damaged brain of the affected mice. The Cxcr4 molecule, therefore, plays a major role in the stroke process and research into drugs that intervene in the process must therefore be a priority in order to prevent the inflammatory reactions during or after a stroke.
