Abstract
There is evidence that the major mediators of stress, i.e., catecholamines and glucocorticoids, play an important role in modulating thymopoiesis and consequently immune responses. Furthermore, there are data suggesting that glucocorticoids influence catecholamine action. Therefore, to assess the putative relevance of glucocorticoid-catecholamine interplay in the modulation of thymopoiesis we analyzed thymocyte differentiation/maturation in non-adrenalectomized and andrenalectomized rats subjected to treatment with propranolol (0.4 mg.100 g body weight-1.day-1) for 4 days. The effects of beta-adrenoceptor blockade on thymopoiesis in non-adrenalectomized rats differed not only quantitatively but also qualitatively from those in adrenalectomized rats. In adrenalectomized rats, besides a more efficient thymopoiesis [judged by a more pronounced increase in the relative proportion of the most mature single-positive TCRalphabetahigh thymocytes as revealed by two-way ANOVA; for CD4+CD8- F (1,20) = 10.92, P < 0.01; for CD4-CD8+ F (1,20) = 7.47, P < 0.05], a skewed thymocyte maturation towards the CD4-CD8+ phenotype, and consequently a diminished CD4+CD8-/CD4-CD8+ mature TCRalphabetahigh thymocyte ratio (3.41 +/- 0.21 in non-adrenalectomized rats vs 2.90 +/- 0.31 in adrenalectomized rats, P < 0.05) were found. Therefore, we assumed that catecholaminergic modulation of thymopoiesis exhibits a substantial degree of glucocorticoid-dependent plasticity. Given that glucocorticoids, apart from catecholamine synthesis, influence adrenoceptor expression, we also hypothesized that the lack of adrenal glucocorticoids affected not only beta-adrenoceptor- but also alpha-adrenoceptor-mediated modulation of thymopoiesis.
Highlights
It is well known that stress causes profound involution of the thymus gland [1]
Propranolol (P < 0.05) affected thymocyte proliferation in non-Adx rats, causing an increase in the percentage of proliferating cells, while it had no effect in Adx rats (Table 1)
The results of the present study showed that a 4-day propranolol treatment has a differential effect on thymus weight and thymocyte yield in non-Adx and Adx rats
Summary
It is well known that stress causes profound involution of the thymus gland [1]. Increased secretion of catecholamines (CAs) and glucocorticoids (GCs), the end-products of the sympatho-adrenal and hypothalamo-pituitary-adrenal (HPA) axes, respectively, is the major trademark of the prototypical stress response [2,3].Ample evidence from denervation and pharmacological studies [4,5,6] has implicated CAs in the fine-tuning of thymopoiesis (reviewed in Ref. 7). It is well known that stress causes profound involution of the thymus gland [1]. Increased secretion of catecholamines (CAs) and glucocorticoids (GCs), the end-products of the sympatho-adrenal and hypothalamo-pituitary-adrenal (HPA) axes, respectively, is the major trademark of the prototypical stress response [2,3]. Ample evidence from denervation and pharmacological studies [4,5,6] has implicated CAs in the fine-tuning of thymopoiesis (reviewed in Ref. 7). There is strong evidence that CAs exert thymus-dependent immunomodulatory effects via β-adrenoceptors (β-ARs) There are data indicating that some of the effects of CAs on the thymus may be mediated via α-ARs [5,9]. GCs have been implicated in the modulation of thymocyte development [12]
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