The Influence of Antiglucocorticoids on Stress and Shocka

Lázár, G.; Husztik, E.; Duda, E.; Agarwal, M.K.

doi:10.1111/j.1749-6632.1995.tb31384.x

Cited by 13 publications

(2 citation statements)

References 40 publications

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“…GC were the first neuroendocrine mediators which were found to be consistently associated with immunosuppression [20][21][22] , and directly modulate immunological functions through GC receptors expressed in cells of the immune system. Thus, it is considered that they are to a greater or lesser degree responsible for the immunosuppression caused by the bulk of stressors 23) .…”

Section: Introductionmentioning

confidence: 99%

Stress- and Aging-Associated Modulation of Macrophage Functions.

Kizaki

Suzuki

Ookawara

et al. 2002

Environ. Health Prev. Med.

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Effects of environmental (cold) stress and aging on cells in monocyte/macrophage lineage were investigated. We demonstrated that immune suppressive states seen in acute cold-stressed mice (8-10 weeks of age) is attributable to Fc1RII bright suppressor macrophages. Serum corticosterone levels were markedly increased in acute cold-stressed mice. In addition, expression of glucocorticoids (GC) receptor mRNA was observed in Fc1RII bright cells from these mice. The increase of Fc1RII bright cells in peritoneal exudate cells caused by acute cold stress was inhibited by adrenalectomy or administration of a saturating amount of the GC antagonist RU 38486 (mifepristone). On the contrary, administration of the GC agonist, dexamethasone, markedly increased the proportion of Fc1RII bright cells in peritoneal exudate cells of control mice. These results suggest that the generation of Fc1RII bright suppressor cells of monocyte/macrophage lineage by acute cold stress was mediated by action of GC through the GC receptor. We likewise found that the proportion of Fc1RII bright suppressor macrophages is increased in aged mice (22-24 months of age). Meanwhile, activated macrophages which function as antigen presenting cells were decreased in aged rats. Both the basal corticosterone concentrations in serum and the expression of mRNA for GC receptor in peritoneal macrophages increased significantly in aged animals, suggesting that these populational and functional changes of macrophages in aged animals were mediated, in part, by the increased basal levels of GC. This is probably being responsible for immunosenescence.

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Section: Introductionmentioning

confidence: 99%

Stress- and Aging-Associated Modulation of Macrophage Functions.

Kizaki

Suzuki

Ookawara

et al. 2002

Environ. Health Prev. Med.

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“…Glucocorticoid (GC) is now recognized to be among the most central of hormones secreted in response to stress after activation of the HPA, and is considered to be of critical importance in the control of homeostasis [2]. On the contrary, GC is also considered to be responsible for the immunosuppression caused by the majority of stressors [3][4][5][6]. Meanwhile, HPA dysfunction is often observed during ageing, and ageing has been defined as a general decline in bodily function associated with a decrease in the ability to maintain homeostasis, i.e.…”

Section: Introductionmentioning

confidence: 99%

Effects of Ageing on Generation of ED2^high Major Histocompatibility Complex Class II⁺ Macrophages During Cold Stress

et al. 2000

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The effects of cold stress (5 degrees C, 24 h) were investigated on the function and surface phenotype of peritoneal cells in the monocyte/macrophage lineage from young (8-10-week-old) and old (22-24-month-old) rats. The role of glucocorticoid (GC) in the immunomodulation by cold stress was also examined. The proportion of cells with a high density of ED2 (ED2high cells), expressing major histocompatibility complex (MHC) class II molecules, was significantly increased in peritoneal cells during cold stress in young, but not in old, rats. Antigen-presenting function was significantly higher in ED2high cells than in cells with a low density of ED2 (ED2low cells), thereby indicating that ED2high cells are at a functionally high level. While serum corticosterone concentration in old rats increased markedly after 3 h of cold stress, that in young rats did not vary substantially, and was followed by a significant decrease in both groups of rats after 24 h of cold stress. Administration of dexamethasone to young rats completely inhibited the increase of ED2high cells caused by cold stress. Meanwhile, the proportion of ED2high cells in young rats was significantly increased by adrenalectomy. Furthermore, nuclear translocation of a large amount of the GC receptor was observed in ED2low cells. These results suggest that cold stress enhances immune function in young rats, but not in old rats, and that the generation of ED2high cells are partly regulated by circulating GC level.

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