The neuropeptide galanin is highly expressed in the central and peripheral nervous system and in the immune system. Not only the immune system but also the activation of the nervous system plays a decisive role in the pathology of inflammatory diseases. Therefore, one can assume, that galanin acts as a neuro-immunological mediator. In fact, it has been shown, that galanin possesses an anti-inflammatory effect on inflammatory diseases. The effects of galanin are mediated via three G-protein-coupled receptors: GAL1, GAL2 and GAL3 receptor. In this thesis the role of the GAL3 receptor in inflammations of the skin and the respiratory tract is examined by using transgenic GAL3-knockout (GAL3-KO) mice. In inflammatory reactions of the skin GAL3-KO mice showed a trend of an increased neutrophil infiltration. In inflamed lung tissue of GAL3-KO mice the expression and concentration of the pro-inflammatory cytokines tumor necrosis factor-α and interleukin-1β did not differ significantly from WT mice. Even though in the current study no significant differences between GAL3-KO and WT mice were observed, an involvement of the GAL3 receptor concerning different parameters in inflammatory diseases of the skin and lung cannot be excluded.