Neurogenic inflammation in the respiratory tract: actions of sensory nerve mediators on blood vessels and epithelium of the airway mucosa

Abstract

Sensory nerves in airways - when stimulated - can mediate a complex set of local tissue changes in addition to their usual reflex responses. These local changes, which are collectively known as neurogenic inflammation, include alterations in mucosal blood flow, increased vascular permeability, leukocyte chemotaxis, and changes in epithelial cell mucus secretion and ion transport. Neuropeptides such as substance P, released by chemically sensitive nerve terminals (irritant receptors), probably initiate the changes, but it is unknown whether these peptides act directly on the target cells or by way of mediator produced by other cells in the airway mucosa. Neurogenic inflammation can be decreased by drugs that interfere with the sensory nerves or their mediators. In contrast, the sensitivity of neurogenic inflammation appears to be increased by naturally occurring airway infections, certain prostaglandins, and glucocorticoids. Thus far, most research on neurogenic inflammation in the respiratory tract has been done on the rat and guinea pig. An important step toward understanding the relevance of neurogenic inflammation in human airway diseases such as asthma will be made by learning the complete spectrum of tissue responses mediated by sensory nerves in the airways of mammals other than rodents.