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Articles in PresS, published online ahead of print April 12, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00363.2001
Submitted on September 12, 2001
Accepted on April 4, 2002
1 Neurobiology and Anatomy, West Virginia University, Morgantown, WV, USA
2 Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV, USA
* To whom correspondence should be addressed. E-mail: zwu{at}hsc.wvu.edu.
Interleukin-1ß(IL-1ß) causes airway inflammation, enhances airway smooth muscle responsiveness and alters neurotransmitter expression in sensory, sympathetic and myenteric neurons. The aim of this study was to examine the role of intrinsic airway neurons in airway hyperresponsiveness (AHR) induced by IL-1[[beta]. Ferrets were instilled intratracheally with IL-1ß(0.3 µg/0.3ml) or saline (0.3 ml) once daily for 5 days. Tracheal smooth muscle contractility in vitro and SP expression in tracheal neurons were assessed. After IL-1ß treatment, tracheal smooth muscle reactivity to acetylcholine (ACh) and methacholine (MCh) was significantly increased (EC50's: 0.91 to 0.37 µM for ACh and 0.43 to 0.20 µM for MCh in control and IL-1ß-treated,respectively), as were smooth muscle contractions to electric field stimulation (EFS) at 10 Hz and 30 Hz. Contractions to EFS were atropine sensitive. The IL-1ß-induced AHR was maintained in tracheal segments cultured for 24 h, a procedure shown to deplete sensory nerves while maintaining viability of intrinsic airway neurons. Pretreatment with CP-99994, an antagonist of neurokinin 1 (NK1)-receptor, attenuated the IL-1ß-induced increase in reactivity to ACh and MCh and to EFS in cultured tracheal segments but had no effect after saline-treatment. The number of SP-containing neurons in longitudinal trunk, SP-innervation of superficial muscular plexus neurons, and SP nerve fiber density in tracheal smooth muscle all increased significantly after treatment with IL-1ß. These results show that the enhanced cholinergic airway smooth muscle contractile responses induced by IL-1ß are mediated by the actions of SP release from intrinsic airway neurons.
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