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Nerve growth factor is released by IL-1ß and induces hyperresponsiveness of the human isolated bronchus

¹ EA 3771, Inflammation and environment in asthma, Université Louis Pasteur, Strasbourg, and ² UPRES EA220, Université de Versailles and UFR Biomédicale des Saints-Pères, and ³ Laboratoire d'anatomo-pathologie Guigui-Georges, Paris, France.

CORRESPONDENCE: N. Frossard, EA 3771Inflammation and environment in asthma, Faculté de pharmacie, Université Louis Pasteur, BP 60024, 67401 Illkirch Cedex, France. Fax: 33 390244309. E-mail: nelly.frossard@pharma.u-strasbg.fr

Keywords: Asthma, bronchial hyperresponsiveness, inflammation, nerve growth factor, neurotrophin

Received: April 23, 2004
Accepted March 16, 2005

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)-1ß. As IL-1ß 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-1ß was able to induce NGF release from isolated bronchi, and whether NGF might participate into IL-1ß-induced AHR.

IL-1ß (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-1ß 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-1ß, 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.

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