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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Nasal IgA secretion in a murine model of acute stress. The possible role of catecholamines.
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Nasal IgA secretion in a murine model of acute stress. The possible role of catecholamines.

机译：急性应激的小鼠模型中的鼻IgA分泌。儿茶酚胺的可能作用。

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Stress stimuli affect the immune system of the mucosa, and in particular IgA secretion. It is well documented that intense psychological and physical stress can increase susceptibility to infection by diverse pathogens in the upper respiratory tract. Our workgroup reported that chronic stress caused by immobilization elicits a decrease in nasal IgA levels in mice. Here, we explore how acute stress (caused by 4 h of immobilization) affects IgA secretion in the nasal mucosa, and the possible role of the sympathetic nervous system in this effect. Nine-week-old male CD1 mice were divided into four groups: control, chemical sympathectomy (with 6-OHDA) and treatment with nadolol (5 mg/kg) or phentolamine (15 mg/kg). All these groups were subdivided into stressed and unstressed animals. The parameters evaluated included plasma corticosterone and epinephrine (only in control groups), SIgA levels (by ELISA) and SIgA expression (by Western Blot) in nasal fluid, percentage of IgA + plasma cells, and mRNA expression of heavy alpha chain, pIgR,TNF alpha and TGF beta in nasal mucosa. Acute stress reduced the percentage of IgA + cells while increasing the levels of IgA, the two hormones, and the mRNA expression of heavy alpha chain, pIgR, TNF alpha and TGF beta, which resulted in greater synthesis and transport of IgA. The treatments with 6-OHDA and alpha- and beta-adrenergic receptor blockers suggest that sympathetic innervation by both types of adrenergic receptors is important for the control of SIgA secretion in nasal mucosa during acute stress. The increase in this parameter depended on the cytokines involved in IgA synthesis and transport. (C) 2014 Elsevier B.V. All rights reserved.
机译：应激刺激影响粘膜的免疫系统，特别是IgA分泌。有充分的证据表明，强烈的心理和身体压力会增加上呼吸道中多种病原体感染的易感性。我们的工作组报告说，固定化引起的慢性应激引起小鼠鼻IgA水平降低。在这里，我们探讨了急性应激（由固定4小时引起）如何影响鼻粘膜中IgA的分泌，以及交感神经系统在此效应中的可能作用。九周龄的雄性CD1小鼠分为四组：对照组，化学交感神经切除术（6-OHDA）和纳多洛尔（5 mg / kg）或苯妥拉明（15 mg / kg）治疗。所有这些组又分为应激动物和非应激动物。评估的参数包括血浆皮质酮和肾上腺素（仅在对照组中），鼻液中的SIgA水平（通过ELISA）和SIgA表达（通过Western Blot），IgA +浆细胞的百分比以及重链α，pIgR的mRNA表达，鼻粘膜中的TNFα和TGFβ。急性应激降低了IgA +细胞的百分比，同时增加了IgA，两种激素以及重链，pIgR，TNFα和TGFβ的mRNA表达，从而导致IgA的合成和转运更高。用6-OHDA以及α-和β-肾上腺素受体阻滞剂进行的治疗表明，两种类型的肾上腺素能受体的交感神经支配对于急性应激期间鼻黏膜中SIgA分泌的控制很重要。该参数的增加取决于参与IgA合成和运输的细胞因子。 （C）2014 Elsevier B.V.保留所有权利。

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