Institute of Experimental Endocrinology, Center of Excellence CENDO and Center of Excellence for Cardiovascular Research, Slovak Academy of Sciences, Bratislava, Slovakia.
Neuroimmunomodulation. 2012;19(2):69-78. doi: 10.1159/000329002. Epub 2012 Jan 11.
Stress-induced rise in circulating catecholamines (CAs), followed by modulation of β-adrenergic receptors (adrenoceptors, ARs), is one of the pathways involved in the stress-mediated effects of immune functions. The spleen is an organ with a high number of lymphocytes and provides a unique microenvironment in which they reside. Thus, lymphocytes may respond differently to CAs in the spleen than in the circulation. No reports exist concerning the involvement of β-ARs in stress-mediated effects on T and B cells isolated from the spleen. Therefore, our aim was to investigate the effect of single stress exposure on gene expression and cellular localization of β-adrenoceptor subtypes in splenic T and B cells. We tried to correlate changes in adrenoceptors with the expression of apoptotic proteins.
Immobilization (IMMO) was used as a stress model. T and B cells were isolated from rat spleen using magnetically labeled antibodies. The gene expression of individual adrenoceptors and apoptotic proteins was evaluated by real-time PCR. Immunofluorescence was used to evaluate localization and adrenoceptor expression.
We have found T cells to be more vulnerable to stress compared to B cells, because of increased β₁-, β₂- and β₃-ARs after a single IMMO. Moreover, β₂-ARs translocated from the nucleus to the plasma membrane in T cells after IMMO. The rise in β-ARs most probably led to the rise of Bax mRNA and Bax to Bcl-2 mRNA ratio. This might suggest the induction of an apoptotic process in T cells.
Higher susceptibility of T cells to stress via modulation of β-ARs and apoptotic proteins might shift the immune responsiveness in the spleen.
应激引起的循环儿茶酚胺（CA）升高，继而调节β-肾上腺素能受体（β-AR），是参与应激介导免疫功能的途径之一。脾脏是淋巴细胞数量较多的器官，为其提供了独特的微环境。因此，淋巴细胞对CA的反应可能与循环系统中的 CA 不同。目前尚无关于β-AR 参与应激对脾脏分离的 T 和 B 细胞的影响的报道。因此，我们的目的是研究单次应激暴露对脾脏 T 和 B 细胞中β-AR 亚型基因表达和细胞定位的影响。我们试图将肾上腺素能受体的变化与凋亡蛋白的表达相关联。
使用固定（IMMO）作为应激模型。使用磁性标记的抗体从大鼠脾脏中分离 T 和 B 细胞。通过实时 PCR 评估个体肾上腺素能受体和凋亡蛋白的基因表达。免疫荧光用于评估定位和肾上腺素能受体表达。
与 B 细胞相比，T 细胞对应激更敏感，因为单次 IMMO 后β₁、β₂和β₃-AR 增加。此外，β₂-AR 在 T 细胞中从核转移到质膜。β-AR 的增加很可能导致 Bax mRNA 和 Bax 与 Bcl-2 mRNA 比值的增加。这可能表明 T 细胞中诱导了凋亡过程。
通过调节β-AR 和凋亡蛋白，T 细胞对压力的敏感性增加可能会改变脾脏的免疫反应性。
