Nerve growth factor (NGF) is a neurotrophic factor essential for the development and survival of neurons, and is also an important mediator of inflammation. It is released by airway cells stimulated by interleukin (IL)-1β. As IL-1β induces airway hyperresponsiveness (AHR) to the tachykinin NK-1 receptor agonist [Sar9,Met(O2)11]-substance P in human isolated bronchi, the aim of this study was to determine whether IL-1β was able to induce NGF release from isolated bronchi, and whether NGF might participate into IL-1β-induced AHR. IL-1β (10 ng·mL-1; 21°C; 15 h) increased the release of NGF from human isolated bronchi in vitro, and, in organ bath studies, the response of human bronchi to [Sar9,Met(O2)11]-substance P (0.1 μm). A significant correlation was found between these responses. AHR induced by IL-1β was abolished by a blocking anti-human NGF antibody. Finally, NGF (1 ng·mL-1; 37°C; 0.5 h) by itself induced a significant increase in [Sar9,Met(O2)11]-substance P responsiveness. By contrast, it did not change the maximal contraction to acetylcholine. In conclusion, the present study clearly demonstrated that nerve growth factor may participate in the airway hyperresponsiveness induced by interleukin-1β, which supports the neuro-immune cross-talk that may be active in the development of hyperresponsiveness in the human airways, and suggests nerve growth factor is active in the airways in asthma. Copyright © ERS Journals Ltd 2005.
Frossard, N., Naline, E., Höglund, C. O., Georges, O., & Advenier, C. (2005). Nerve growth factor is released by IL-1β and induces hyperresponsiveness of the human isolated bronchus. European Respiratory Journal, 26(1), 15–20. https://doi.org/10.1183/09031936.05.00047804