Immune mediated depressive behaviour: causes, consequences and therapeutic opportunities

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Depression is one of the most disabling diseases, affecting 340 million people worldwide. Besides occuring spontaneously, depressive symptoms are frequently associated with chronic immunological diseases such as inflammatory rheumatic diseases, inflammatory bowel disease, asthma or infectious diseases. Consistently, a therapeutically induced activation of the peripheral immune system can lead to the development of a depressive behaviour. This can been observed e.g. in patients with hepatitis C upon treatment with recombinant interferon (IFN)-a. Thus, IFN-a therapy offers a promising experimental model for prospectively studying mechanisms of immune mediated depressive behaviour in humans, which we are planning to combine in the present study with a mouse model on IFN-a induced depressive behaviour. According to our hypothesis, depressive behaviour is the consequence of a defined peripheral immunological dysequilibrium, leading to an ill-routed body-brain cross talk. Immune mediators involved likely comprise cell adhesion molecules, chemokines/cytokines and mechanisms of immune tolerance, e.g. indoleamine 2,3- dioxygenase. The delineation of key mediators enclosed in this ill-routed body-brain cross talk is the aim of the present study. Such insights will provide an in depth understanding on signalling pathways between body and mind and will subsequently foster future research to improve therapeutical efficiency not only with respect to spontaneously occuring depression, but also depressive behaviour triggered by chronic immunological diseases.