Neuroimmunologic control of asthma

Published

Journal Article (Review)

The neural, neuroendocrine, and immune systems frequently are believed to be completely separate entities; however, evidence suggests that these systems interact extensively to modulate pulmonary immune responses. The functional significance of these interactions suggests that many pulmonary responses to proinflammatory stimuli are regulated by the neural and neuroendocrine systems. There is no clear delineation between the pulmonary proinflammatory responses that strictly result from the classic inflammatory cells and their mediators and those responses that largely are amplified by neuropeptides and other neural- or neuroendocrine-derived mediators. This viewpoint highlights the inherent complexity of the lung's proinflammatory responses and has implications for novel therapeutic approaches. In clinical trials, specific targeting of one component of the pulmonary inflammatory response is likely to have only limited success. Therapies that target several distinct pathways that have been implicated in these inflammatory responses are likely to be the most effective in controlling asthma. This concept of broad-spectrum targeting likely explains the effectiveness of nonspecific therapies, such as steroids, which affect multiple pathways of neuroimmune responses. It has become a priority to gain appreciation of the neuroimmunologic regulation of asthma and other forms of chronic inflammatory lung disease. Understanding such collaborating systems in development, health, and disease is a powerful paradigm for the future for elucidation of the pathophysiology of inflammatory lung diseases and for novel therapeutic approaches that could benefit patients.

Full Text

Duke Authors

Cited Authors

  • Haley, KJ; Sunday, ME

Published Date

  • November 1, 2002

Published In

Volume / Issue

  • 22 / 4

Start / End Page

  • 807 - 825

International Standard Serial Number (ISSN)

  • 0889-8561

Digital Object Identifier (DOI)

  • 10.1016/S0889-8561(02)00023-1

Citation Source

  • Scopus