Allergic asthma is characterized by chronic inflammation in the airways, development of hyperreactivity and recurrent reversible bronchial obstruction of the airways. Target cells that are responsible for airway hyperreactivity, oburation, and acute inflammation in the airways are, among others, motor and sensory neurons as well as epithelial and airway smooth muscle cells.

Studies performed in vitro, and in vivo on animal model and in humans were fundamental in formulation of neurogenic hypothesis of inflammation in asthma. Factors mediating in neuroimmunological interactions are neurotrophic factors produced in the site of inflammation. The are able to modulate severity of airway hyperreactivity and intensity of neurogenic inflammation which was confirmed by altered expression profile of neurotrophins in patients with alergic inflammation. Increased neurotrophin levels were also observed in patients with other immunological diseases (including atopic diseases) both locally (in the airways) and peripherally (in blood), which additionally confirms their role in the development of airway inflammation in asthma. Recent studies indicate increasing interest in the involvement of neurogenic inflammation in asthma and the better understanding in this field may facilitate more precise diagnosis of asthma in future.