Neurogenic Inflammation in Allergic Disease

There is a close association between the allergic inflammatory response and neural control mechanisms. Inflammatory products may activate sensory nerves to cause symptoms, such as cough and chest tightness, sneezing, and itching, which are among the most troublesome aspects of allergic diseases. Sensory nerves themselves may also release neurotransmitters that increase inflammation, and this is termed neurogenic inflammation. The phenomenon of neurogenic inflammation is well established in the skin and in the respiratory tract of rodents, although there is less certainty about its role in human airway diseases. The peptides substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP) are localized to a population of sensory neurons in the respiratory tract and the skin (1–4). These peptides have potent effects on the circulation, secretions, airway smooth muscle tone, and inflammatory and immune cells. Although some clues to the physiological and pathophysiological role of sensory neuropeptides are provided by their localization and functional effects, their role in allergic diseases will only become apparent when specific inhibitors are used in clinical studies. Depletion studies using capsaicin have proved to be very helpful in elucidating the role of sensory neuropeptides in animal models, but the recent development of specific receptor antagonists and other inhibitors is proving to be critical in understanding the role of neurogenic inflammation in the respiratory tract and skin. Most studies have concentrated on the lower airways and asthma (5),but there is increasing information about the nose and skin (4,6).