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广泛性焦虑症患者单核细胞中苯二氮䓬诱导的趋化性受损。

Benzodiazepine-induced chemotaxis is impaired in monocytes from patients with generalized anxiety disorder.

作者信息

Sacerdote P, Panerai A E, Frattola L, Ferrarese C

机构信息

Department of Pharmacology, University of Milano, Italy.

出版信息

Psychoneuroendocrinology. 1999 Feb;24(2):243-9. doi: 10.1016/s0306-4530(98)00079-1.

Abstract

Peripheral benzodiazepine receptors (PBR) modulate chemotaxis and cytokine production of monocytes and lymphocytes. Since PBR are decreased in animal models of stress and in patients with anxiety disorders, in the present study we analyze the ability of monocytes obtained from patients suffering from generalized anxiety to migrate towards chemoattracting benzodiazepines. In these patients, the benzodiazepine-induced chemotaxis is completely abolished, while the response to the control chemoattractant formyl-leu-met-phe is still maintained. The chemotaxis responses are not restored after pharmacological treatment of the pathology. The decreased chemotactic response could be linked to a decreased number of PBR receptors present on monocytes of generalized anxiety disorder patients.

摘要

外周苯二氮䓬受体(PBR)调节单核细胞和淋巴细胞的趋化性及细胞因子生成。由于在应激动物模型和焦虑症患者中PBR减少,在本研究中,我们分析了从广泛性焦虑症患者获取的单核细胞向趋化性苯二氮䓬迁移的能力。在这些患者中,苯二氮䓬诱导的趋化性完全丧失,而对对照趋化剂甲酰-亮氨酰-甲硫氨酰-苯丙氨酸的反应仍保持。病理经药物治疗后,趋化性反应未恢复。趋化性反应降低可能与广泛性焦虑症患者单核细胞上PBR受体数量减少有关。

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