Acute stress differently modulates ß1, ß2 and ß3 adrenoceptors in T cells, but not in B cells, from the rat spleen.

OBJECTIVES: Stress-induced rise in circulating catecholamines (CAs), followed by modulation of ß-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 ß-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 ß-adrenoceptor subtypes in splenic T and B cells. We tried to correlate changes in adrenoceptors with the expression of apoptotic proteins. METHODS: 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. RESULTS: We have found T cells to be more vulnerable to stress compared to B cells, because of increased ß1-, ß2- and ß3-ARs after a single IMMO. Moreover, ß2-ARs translocated from the nucleus to the plasma membrane in T cells after IMMO. The rise in ß-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. CONCLUSION: Higher susceptibility of T cells to stress via modulation of ß-ARs and apoptotic proteins might shift the immune responsiveness in the spleen.