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The role of neurotrophins in bronchial asthma: contribution of the pan-neurotrophin receptor p75.

机译:神经营养蛋白在支气管哮喘中的作用:泛神经营养蛋白受体p75的贡献。

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摘要

Allergic bronchial asthma is characterized by chronic inflammation of the airways, development of airway hyperreactivity and recurrent reversible airway obstruction. Target and effector cells responsible for airway hyperresponsiveness and airway obstruction include sensory and motor neurons as well as epithelial and smooth muscle cells. Although it is well established that the inflammatory process is controlled by T-helper-2 (Th2) cells, the mechanisms by which immune cells interact with neurons, epithelial cells or smooth muscle cells still remain uncertain. Due to growing evidence for extensive communication between neurons and immune cells, the mechanisms of this neuroimmune crosstalk in lung and airways of asthmatic patients are becoming the focus of asthma research. Neurotrophins represent molecules potentially responsible for regulating and controlling the crosstalk between the immune and peripheral nervous system. They are constitutively expressed by resident lung cells and produced in increasing concentrations by immune cells invading the airways under pathological conditions. Neurotrophins modify the functional activity of sensory and motor neurons, leading to enhanced and altered neuropeptide and tachykinin production. These effects are defined as neuronal plasticity. The consequences are the development of neurogenic inflammation.
机译:过敏性支气管哮喘的特征是气道慢性炎症,气道反应过度和反复可逆性气道阻塞。引起气道高反应性和气道阻塞的靶标和效应细胞包括感觉和运动神经元,以及上皮和平滑肌细胞。尽管已经公认炎症过程受T-helper-2(Th2)细胞控制,但免疫细胞与神经元,上皮细胞或平滑肌细胞相互作用的机制仍然不确定。由于越来越多的证据表明神经元与免疫细胞之间广泛的交流,哮喘患者的肺和气道中这种神经免疫串扰的机制正成为哮喘研究的重点。神经营养蛋白代表潜在地负责调节和控制免疫系统与周围神经系统之间的串扰的分子。它们由驻留的肺细胞组成性表达,并在病理条件下由侵入气道的免疫细胞以增加的浓度产生。神经营养蛋白修饰感觉和运动神经元的功能活性,导致增强和改变的神经肽和速激肽的产生。这些作用定义为神经元可塑性。结果是神经性炎症的发展。

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