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Spitzenmedizin mit Herz


AG Thrombozyten und Inflammation


Research Group "Platelets in Inflammation" (Daniel Duerschmied, MD)

We investigate the contribution of platelets to acute and chronic inflammatory reactions. Among other things, we are looking for new approaches to improve the therapy of reperfusion damage after myocardial infarction. Our long-term goal is to use basic research projects to identify innovative biomarkers and therapeutic options and to verify them in patients. We also develop our own clinical studies for this purpose, which we carry out partly as a single center and partly jointly with other centers.

Blood platelets not only orchestrate hemostasis and (athero-) thrombosis, but also fulfill a broad variety of functions in the immune system. Platelets circulate through the body in a quiescent state, ready to interact with the vessel wall after injury or inflammatory challenge. They are prepared to rapidly interact with neutrophils, monocytes/macrophages, lymphocytes, and with endothelial cells to promote the recruitment of immune cells into inflamed tissues, to control cytokine release, and in some cases trap and kill pathogens.

Platelets store a multitude of different factors in their granules, which can be released within seconds after stimulation. One of the secreted factors is serotonin. Some of our research efforts focus on this biogenic amine not (only) because it has been dubbed the "happiness hormone", but because we are convinced that it is an important modulator of many immune functions. Platelets store serotonin in their dense granules at mM concentrations and secrete it upon activation.

One focus of our work is to decipher mechanisms of platelet serotonin action in inflammatory settings. We found that isolated serotonin receptor stimulation greatly decreases platelet adhesion due to shedding of glycoprotein Ibα from the surface. Platelets are therefore unable to incorporate into growing arterial thrombi after serotonergic stimulation. Interestingly, this involves the activation of tumor necrosis factor-α converting enzyme (TACE), an enzyme that is also an important player in inflammation.

We also discovered that platelet serotonin affects the recruitment of immune cells to sites of inflammation e.g. in mouse models of endotoxic shock or sterile peritonitis. In line with this, survival of lipopolysaccharide-induced endotoxic shock is improved in the absence of platelet serotonin. Furthermore increased plasma serotonin concentrations (after acute treatment with the selective serotonin reuptake inhibitor fluoxetine) in mice promote leukocyte-endothelial interactions, suggesting that serotonin is a promoter of acute inflammation.

In a mouse model of myocardial infarction (LAD ligation) we observed that myocardial necrosis is attenuated when platelet serotonin is absent (Tph1 k.o. or chronic fluoxetine treatment). This was accompanied by an improved heart function. Serotonin seems to worsen the inflammatory profile in the heart after myocardial infarction and increases neutrophil infiltration. Mechanistically serotonin induces neutrophil degranulation thereby rapidly upregulating CD11b surface expression in murine and human neutrophils. These findings provide a rationale for targeting serotonin to ameliorate the inflammatory response in myocardial reperfusion injury.

Prof. Dr. med. Dürschmied


Telefon: +49 761 270-70470
Telefax: +49 761 270-70450