Despite recent advances in the development of anti-asthmatic medication, asthma continues to be a major health problem worldwide. The symptoms of asthmatic patients include wheezing, chest tightness, cough and shortness of breath, which, together with airway hyperresponiveness, previously have been attributed to a dysfunction of airway nerves. However, research in the last two decades identified Th2-sensitization and the subsequent allergic reaction to innocuous environmental antigens as a basic immunological mechanism leading to chronic airway inflammation. Recent evidence suggests that the development of allergic asthma is influenced by events and circumstances in early childhood and even in utero. Allergen, ozone or stress exposure, as well as RSV infection in early life could be able to induce irreversible changes in the developing epithelial-mesenchymal trophic unit of the airways. The co-existence of chronic inflammation and neural dysfunction have recently drawn attention to the involvement of interaction pathways between the nervous and the immune system in the airways. Intensive basic research has accumulated morphological as well as functional evidence for the interaction between nerves and immune cells. Neuropeptides and neurotrophins have come into focus of attention as the key mediators of neuro-immune interactions, which lead to the development of several pharmacological compounds specifically targeting these molecules. This review will integrate our current knowledge on the involvement of neuro-immune pathways in asthma on the cellular and molecular level. It will summarize the results of pharmacological studies addressing the potential of neuropeptides and neurotrophins as novel therapeutic targets in asthma.