Nassenstein C, Kutschker J, Tumes D, Braun A
Immunology and Allergology, Fraunhofer Institute of Toxicology and Experimental Medicine, Nikolai-Fuchs-Strasse 1, Hannover, Germany.
Biochem Soc Trans. 2006 Aug;34(Pt 4):591-3. doi: 10.1042/BST0340591.
The nature of persistent airway hyperreactivity and chronic inflammation in asthma remains unclear. It has been suggested that bi-directional neuro-immune interaction plays an important role in the pathogenesis of this disease, leading to enhanced airway narrowing after contact with unspecific stimuli, as well as infiltration, activation and degranulation of several immune cell subtypes. Important mediators in neuro-immune cross-talk are neurotrophins, which are produced by cells at the site of inflammation. In addition to modulating the function of several leucocyte subsets, they play an important role in the synthesis of neuropeptides by sensory nerve cells. Neuropeptides have been shown to cause smooth-muscle contraction and, in addition, modulate the production of pro-inflammatory molecules by leucocytes. The aim of the present review is to provide an overview of the molecular mechanisms by which neurotrophins and neuropeptides are involved in neuro-immune cross-talk in allergic asthma.
哮喘中持续性气道高反应性和慢性炎症的本质仍不清楚。有人提出，双向神经免疫相互作用在该疾病的发病机制中起重要作用，导致接触非特异性刺激后气道狭窄加剧，以及几种免疫细胞亚型的浸润、激活和脱颗粒。神经免疫相互作用中的重要介质是神经营养因子，它们由炎症部位的细胞产生。除了调节几种白细胞亚群的功能外，它们在感觉神经细胞合成神经肽中也起重要作用。神经肽已被证明可引起平滑肌收缩，此外，还可调节白细胞产生促炎分子。本综述的目的是概述神经营养因子和神经肽参与过敏性哮喘神经免疫相互作用的分子机制。
