Xing Hong, Ling Jennifer X, Chen Meng, Johnson Richard D, Tominaga Makoto, Wang Cong-Yi, Gu Jianguo
Department of Oral & Maxillofacial Surgery and Diagnostic Sciences, McKnight Brain Institute and College of Dentistry, University of Florida, Gainesville, Florida 32610, USA.
Mol Pain. 2008 Jun 5;4:22. doi: 10.1186/1744-8069-4-22.
Breathing cold air without proper temperature exchange can induce strong respiratory autonomic responses including cough, airway constriction and mucosal secretion, and can exacerbate existing asthma conditions and even directly trigger an asthma attack. Vagal afferent fiber is thought to be involved in the cold-induced respiratory responses through autonomic nerve reflex. However, molecular mechanisms by which vagal afferent fibers are excited by cold remain unknown. Using retrograde labeling, immunostaining, calcium imaging, and electrophysiological recordings, here we show that a subpopulation of airway vagal afferent nerves express TRPM8 receptors and that activation of TRPM8 receptors by cold excites these airway autonomic nerves. Thus activation of TRPM8 receptors may provoke autonomic nerve reflex to increase airway resistance. This putative autonomic response may be associated with cold-induced exacerbation of asthma and other pulmonary disorders, making TRPM8 receptors a possible target for prevention of cold-associated respiratory disorders.
在没有适当温度交换的情况下吸入冷空气会引发强烈的呼吸自主反应,包括咳嗽、气道收缩和粘膜分泌,并会加重现有的哮喘病情,甚至直接引发哮喘发作。迷走传入纤维被认为通过自主神经反射参与寒冷诱导的呼吸反应。然而,迷走传入纤维被寒冷激活的分子机制仍不清楚。通过逆行标记、免疫染色、钙成像和电生理记录,我们在此表明,气道迷走传入神经的一个亚群表达TRPM8受体,寒冷激活TRPM8受体可兴奋这些气道自主神经。因此,TRPM8受体的激活可能引发自主神经反射,增加气道阻力。这种假定的自主反应可能与寒冷诱发的哮喘和其他肺部疾病加重有关,使得TRPM8受体成为预防与寒冷相关的呼吸系统疾病的一个可能靶点。