Mast cells, eosinophils and NANC-nerves in viral respiratory tract infections

Airway hyperresponsiveness to bronchoconstrictor mediators is a main characteristic in the majority of asthmatic patients and correlates well with the severity of the disease. The accumulation of mast cells and eosinophilic leukocytes is a prominent feature of the inflammatory reactions which occur in asthma. In contrast, these cells have received little attention in persons with a viral respiratory tract infection. The increase in the numbers or activities of mast cells and eosinophils is important since it correlates in time with bronchial hyperresponsiveness. Viral respiratory infections can induce airway hyperresponsiveness in humans and animals and can worsen asthmatic reactions. This article reviews current opinions on the relationship between mast cell and eosinophil accumulation/activation and the development of airway hyperresponisiveness after a viral infection. Possible candidates (histamine, interleukin-5 and eotaxin) that can attract or activate eosinophils in the airways are discussed. The precise mechanism by which mast cells and eosinophils contribute to bronchial hyperresponsiveness is at present unknown. Sensory neuropeptides could be important mediators and may be the final, further downstream, common pathway after mast cell and eosinophil infiltration/activation in inducing airway hyperresponsiveness due to respiratory viral infections. In conclusion, during viral infections there is an infiltration/activation of mast cells and eosinophils in the airways. Inflammatory mediators can cause epithelial damage and lead to stimulation of sensory neuropeptides which in turn can lead to airway hyperresponsiveness.