Continuous in vivo treatment with catecholamines suppresses in vitro reactivity of rat peripheral blood T-lymphocytes via α-mediated mechanisms

Felsner, P.; Hofer, Doris; Rinner, I.; Mangge, Harald; Gruber, Martin J.; Korsatko, W.; Schauenstein, Konrad

doi:10.1016/0165-5728(92)90154-d

Cited by 60 publications

(19 citation statements)

References 37 publications

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“…25 Indeed, a recent in vivo study indicates that rats treated with norepinephrine show decreased T lymphocyte responses. 26 We conclude that lymphocytes have the capacity to synthesize dopamine. In addition, we provide evidence for catecholamines being potent inhibitors of different stages in T and B lymphocyte activation.…”

Section: Discussionmentioning

confidence: 99%

Catecholamines are synthesized by mouse lymphocytes and regulate function of these cells by induction of apoptosis

Josefsson

Bergquist²,

Ekman³

et al. 1996

Immunology

231

135

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SUMMARYThe immune and the nervous systems are anatomically closely related and interact with each other by molecules common to both systems, such as cytokines and neurotransmitters. The purpose of this study was to investigate the participation of catecholamines in the neuroimmunological network. The ability of immune cells to produce catecholamines was examined by a highly sensitive capillary electrophoresis assay, which permits detection of easily oxidized catecholamines in the zeptomole (10 ÿ 21 ) range. In addition, the effects of catecholamines on in vitro proliferation, differentiation and apoptosis of lymphocytes were assessed. Mouse spleen cells and macrophages contained on average 7 2 10 ÿ 17 and 2 2 10 ÿ 17 mole dopamine per cell, respectively. In the former cell population also norepinephrine was found. Several mouse B-and T-cell hybridomas were also shown to contain endogenously produced dopamine in levels ranging from 7 2 10 ÿ 20 to 2 2 10 ÿ 18 mole dopamine per cell. In addition, one of the T-cell hybridomas proved to synthesize norepinephrine. The dopamine production of lymphocytes was blocked by the tyrosine hydroxylase inhibitor a -methyl-p-tyrosine, whereas incubation with the precursor L-DOPA increased the dopamine content. Incubation with L-DOPA, dopamine and norepinephrine dose-dependently suppressed mitogen induced proliferation and differentiation of mouse lymphocytes. Even short-time pretreatment of lymphocytes with L-DOPA and dopamine strongly suppressed lymphocyte proliferation and cytokine production. Incubation of lymphoid cells with L-DOPA, dopamine and norepinephrine dose-dependently induced apoptosis which, at least partly, explains the suppressive effects of catecholamines on lymphocyte function. Our results demonstrate that catecholamines: (i) are actively produced by lymphocytes and (ii) have the capacity to act as auto-and/or paracrine regulators of lymphocyte activity through induction of apoptosis.

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Section: Discussionmentioning

confidence: 99%

Catecholamines are synthesized by mouse lymphocytes and regulate function of these cells by induction of apoptosis

Josefsson

Bergquist²,

Ekman³

et al. 1996

Immunology

231

135

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“…In rats, catecholamines administered concomitantly with a ß-blocker exert in vivo a marked suppressive effect on the ex vivo T and B cell mitogen response of peripheral blood lymphocytes (PBL), via ·2-subtype receptors [44]. Since the immunosuppressive activity of the specific ·2-agonist clonidine turned out to be likewise dependent on the concomitant treatment with ß-blockers, it has been suggested that melatonin, released from the pineal gland mainly via ß-adrenergic stimulation [45], could be an endogenous immunoprotective mediator [46].…”

Section: Melatonin As An Immunomodulatormentioning

confidence: 99%

Melatonin Involvement in Immunity and Cancer

Fraschini¹,

Demartini²,

Esposti³

et al. 1998

Neurosignals

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The most studied endocrine product of the pineal gland, melatonin, has been reported to be involved in the feedback between neuroendocrine and immune functions and to exert oncostatic action, at least in certain experimental conditions. Melatonin seems to be an integral part of the immune system, by exerting direct and/or indirect stimulatory effects on both cellular and humoral immunity. Likewise, an antitumor activity of melatonin has been shown in several experimental models in vivo and in vitro. The means by which melatonin exerts its effects on immunity and neoplastic growth have not been elucidated. The different putative mechanisms of action of melatonin investigated so far are here briefly discussed.

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“…NE has been shown to activate TH2 cell-dependent antibody response in vivo [9] , and in combination with IL-12, was shown to increase the pool of TH1 cells [16] . In contrast, NE was reported to suppress proliferation of rat peripheral blood T-lymphocytes [17] (which may be related to catecholamine-induced apoptosis [18] ), decrease IL-2 production by murine splenic naïve CD4+ T cells [19] , and inhibit IFN-γ synthesis by PHAstimulated splenic cells [20] . Additionally, A significant suppression of IL-1, IL-2, IL-4, and IFN-γ interferon production by splenic leukocytes, and proliferative response of splenic T lymphocytes following immunization with sheep red blood cells, was observed in the reeler (rl/rl) mice (a neurologic mutant strain with an abnormally high concentration of cerebellar NE) [21] .…”

Section: Discussionmentioning

confidence: 99%

In vitro Activation of Human and Rat Lymphocyte and Macrophage Functions by Norepinephrine

Gómez-Flores¹,

Caballero‐Hernández²,

Weber³

et al. 2005

American J. of Immunology

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Norepinephrine (NE) has been associated not only with increasing blood pressure, atherosclerosis, heart disease, and other life threatening conditions, but also with altering immune responses by influencing leukocyte functions. In the present study, we evaluated the in vitro effects of NE on rat thymic lymphocyte and human peripheral blood mononuclear cells (HPBMC) functions. We observed that NE marginally, but significantly (P < 0.01) enhanced (1.3-fold increase) proliferation of rat thymic lymphocytes at 10 -5 M, without altering HPBMC proliferation, as compared with untreated control. In addition, NE (10 -5 M) significantly (P < 0.01) enhanced nitric oxide production (2.9 + 0.095 nmol/well) (which reduced 20% cell viability), and stimulated (P < 0.01) TNF-α production (4 + 0.16 pg/ml) by rat macrophages. NE (10 -5 M) was also observed to induce 2-fold increase in mRNA signal of TNF-α, and stimulated that of IL-1 and IL-6 by HPBMC, as compared with untreated control. Taken together, these results indicated that NE was capable to activate in vitro rat and human lymphocyte and macrophage pro-inflammatory response.

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Continuous in vivo treatment with catecholamines suppresses in vitro reactivity of rat peripheral blood T-lymphocytes via α-mediated mechanisms

Cited by 60 publications

References 37 publications

Catecholamines are synthesized by mouse lymphocytes and regulate function of these cells by induction of apoptosis

Catecholamines are synthesized by mouse lymphocytes and regulate function of these cells by induction of apoptosis

Melatonin Involvement in Immunity and Cancer

In vitro Activation of Human and Rat Lymphocyte and Macrophage Functions by Norepinephrine

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