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肺癌是主要医学难题之一,尽管分子生物学和药理学技术在进步,肺癌的治疗结果却不尽人意。临床上,炎症与肿瘤密切相关,炎症能够促进肿瘤的形成。从遗传角度讲,这两个过程受到同一个基因座的调控。越来越多的证据表明,神经和免疫两个系统存在交互作用,其中迷走神经起着重要作用。在临床及动物实验中分别观察到:切除迷走神经后肺部的肿瘤发生率增高,转移增加。表明迷走神经具有保护作用,能抑制肿瘤生长。气道感受器是生物感应器,能感受肺部炎症及肿瘤生长过程中的多种介质和细胞因子。这些信号通过迷走神经传递给脑,提供肿瘤生长的信息,随后产生一系列的反应调节炎症的广度和强度以及肿瘤生长速度。肿瘤细胞表达神经递质的受体,能提供底物与神经元直接相互作用。因此,免疫反应的神经调节既可以靶向炎症又可以靶向肿瘤。认识肺部神经如何监控肿瘤的生长并且产生神经免疫相互作用以调节肿瘤的进展及转移,将提高肺癌的治疗水平。
Lung cancer is one of the major medical problems. Although molecular biology and pharmacology are improving, the treatment of lung cancer is unsatisfactory. Clinically, inflammation and cancer are closely related, inflammation can promote the formation of tumors. From a genetic point of view, these two processes are regulated by the same locus. There is a growing body of evidence that there is an interaction between the two systems of the nerve and the immune system, of which the vagus nerve plays an important role. In clinical and animal experiments were observed: the excision of the vagus nerve after the lung cancer increased incidence of metastasis. Show vagal nerve has a protective effect, can inhibit tumor growth. Airway receptors are biological sensors that can sense various mediators and cytokines in lung inflammation and tumor growth. These signals are passed through the vagus nerve to the brain to provide information on the growth of the tumor, followed by a series of responses that regulate the breadth and intensity of the inflammation and the rate of tumor growth. Tumor cells express neurotransmitter receptors that provide direct interaction of the substrate with neurons. Therefore, the neuromodulation of the immune response can both target inflammation and target tumors. Knowing how the lung nerves monitor tumor growth and produce neuroimmunological interactions to regulate tumor progression and metastasis will increase the level of lung cancer treatment.