Effects of inflammatory cells on neuronal M2 muscarinic receptor function in the lung
Effects of inflammatory cells on neuronal M2 muscarinic receptor function in the lung
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DOI：
10.1016/s0024-3205(98)00587-6
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发表时间：
1999-01-08
期刊：
影响因子：
6.1
通讯作者：
Jacoby, DB
中科院分区：
文献类型：
--
作者：
Fryer, AD;Adamko, DJ;Jacoby, DB
在肺中，从副交感神经释放的乙酰胆碱刺激气道平滑肌上的M-3毒蕈碱受体，诱导收缩和支气管收缩。从这些神经释放的乙酰胆碱的量在局部受到神经元M-2毒蕈碱受体的限制。这些神经元受体在哮喘和哮喘动物模型中功能障碍。M-2毒蕈碱受体功能降低导致乙酰胆碱释放增加和气道高反应性。炎症长期以来与高反应性相关，并且已经研究了炎性细胞在神经元M-2受体功能丧失中的作用。神经元M-2受体功能丧失有几种不同的机制。这些包括内源性拮抗剂如嗜酸性粒细胞主要碱性蛋白的阻断，病毒感染或暴露于促炎细胞因子如γ干扰素后M-2受体表达降低。最后，乙酰胆碱对这些受体的亲和力可以通过暴露于神经氨酸酶而降低。
In the lungs, acetylcholine released from the parasympathetic nerves stimulates M-3 muscarinic receptors on airway smooth muscle inducing contraction and bronchoconstriction. The amount of acetylcholine released from these nerves is limited locally by neuronal M-2 muscarinic receptors. These neuronal receptors are dysfunctional in asthma and in animal models of asthma Decreased M-2 muscarinic receptor function results in increased release of acetylcholine and in airway hyperreactivity. Inflammation has long been associated with hyperreactivity and the role of inflammatory cells in loss of neuronal M-2 receptor function has been examined. There are several different mechanisms for loss of neuronal M-2 receptor function. These include blockade by endogenous antagonists such as eosinophil major basic protein, decreased expression of M-2 receptors following infection with viruses or exposure to pro inflammatory cytokines such as gamma interferon. Finally, the affinity of acetylcholine for these receptors can be decreased by exposure to neuraminidase.