The involvement of central nervous system histamine receptors in psychological stress-induced exacerbation of allergic airway inflammation in mice
The involvement of central nervous system histamine receptors in psychological stress-induced exacerbation of allergic airway inflammation in mice
复制标题
中枢神经系统组胺受体参与心理应激诱发小鼠过敏性气道炎症恶化的研究
DOI：
10.1016/j.alit.2016.05.015
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发表时间：
2016
影响因子：
6.8
通讯作者：
Ohno I.
中科院分区：
文献类型：
--
作者：
Miyasaka T;Okuyama-Dobashi K;Masuda C;Iwami S;Sato M;Mizoguchi H;Kawano T;Ohkawara Y;Sakurada S;Takayanagi M;Ohno I.
背景心理应激是哮喘急性发作的主要危险因素之一。尽管脑中组胺作为与心理应激相关的兴奋性和抑制性神经递质发挥作用，但脑组胺在心理应激诱导的哮喘恶化中的作用仍不清楚。本研究的目的是探讨中枢组胺受体在应激诱发哮喘加重中的作用。方法通过监测支气管肺泡灌洗液中炎性细胞数量和白细胞介素（IL）-13水平、气道对吸入乙酰甲胆碱的反应性、气道上皮细胞粘液分泌、依匹斯汀治疗应激性哮喘小鼠模型血清中抗原特异性IgE含量（一种H1 R拮抗剂），硫哌丁胺结果与用溶剂处理的小鼠相比，用依匹斯汀处理的应激小鼠中应激诱导的哮喘恶化的所有指标均显著降低，而硫代哌丁胺治疗并没有减少炎症细胞在stress.ConclusionsThese结果表明，H1 R，但不是H3/4 R，可能参与应激诱导的哮喘急性发作在中枢神经系统。
BackgroundPsychological stress is one of the major risk factors for asthma exacerbation. Although histamine in the brain acts as an excitatory and inhibitory neurotransmitter associated with psychological stress, the contribution of brain histamine to psychological stress-induced exacerbation of asthma remains unclear. The objective of this study was to investigate the role of histamine receptors in the CNS on stress induced asthma aggravation.MethodsWe monitored the numbers of inflammatory cells and interleukin (IL)-13 levels in bronchoalveolar lavage fluid, airway responsiveness to inhaled methacholine, mucus secretion in airway epithelial cells, and antigen-specific IgE contents in sera in a murine model of stress-induced asthma treated with epinastine (an H 1 R antagonist), thioperamide (an H 3/4 R antagonist), or solvent.ResultsAll indicators of stress-induced asthma exacerbation were significantly reduced in stressed mice treated with epinastine compared with those treated with solvent, whereas treatment with thioperamide did not reduce the numbers of inflammatory cells in the stressed mice.ConclusionsThese results suggest that H 1 R, but not H 3/4 R, may be involved in stress-induced asthma exacerbations in the central nervous system.