Adrenergic suppression of peripheral blood T cell reactivity in the rat is due to activation of peripheral α2-receptors

Felsner, P.; Hofer, Doris; Rinner, I.; Porta, S.; Korsatko, W.; Schauenstein, Konrad

doi:10.1016/0165-5728(94)00158-k

Cited by 60 publications

(32 citation statements)

References 35 publications

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“…In contrast to the well-established expression of b-adrenoceptors in lymphocytes (58), only a few studies have postulated, using indirect methods, the presence of a-adrenoceptors in mononuclear peripheral blood cells (10,33,55,56). Their presence has also been suggested, similarly by indirect evidence, in human neutrophils (35).…”

Section: Discussionmentioning

confidence: 95%

“…The a2-adrenoceptor subtypes a2A, a2B, and a2C mediate some of the biological effects induced by endogenous catecholamines, both in the CNS (53,54) and in a variety of peripheral tissues and cell types, including platelets (30) and leukocytes (35,55,56). Research on genetically deficient animals has clarified the biological roles of these receptors, which seem to be centered in the control of nociception and blood pressure (2).…”

Section: Discussionmentioning

confidence: 99%

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Prevention of Neutrophil Extravasation by α2-Adrenoceptor–Mediated Endothelial Stabilization

Herrera-García

Domínguez-Luis

Arce-Franco

et al. 2014

The Journal of Immunology

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Adrenergic receptors are expressed on the surface of inflammation-mediating cells, but their potential role in the regulation of the inflammatory response is still poorly understood. The objectives of this work were to study the effects of α2-adrenergic agonists on the inflammatory response in vivo and to determine their mechanism of action. In two mouse models of inflammation, zymosan air pouch and thioglycolate-induced peritonitis models, the i.m. treatment with xylazine or UK14304, two α2-adrenergic agonists, reduced neutrophil migration by 60%. The α2-adrenergic antagonist RX821002 abrogated this effect. In flow cytometry experiments, the basal surface expression of L-selectin and CD11b was modified neither in murine nor in human neutrophils upon α2-agonist treatment. Similar experiments in HUVEC showed that UK14304 prevented the activation-dependent upregulation of ICAM-1. In contrast, UK14304 augmented electrical resistance and reduced macromolecular transport through a confluent HUVEC monolayer. In flow chamber experiments, under postcapillary venule-like flow conditions, the pretreatment of HUVECs, but not neutrophils, with α2-agonists decreased transendothelial migration, without affecting neutrophil rolling. Interestingly, α2-agonists prevented the TNF-α–mediated decrease in expression of the adherens junctional molecules, VE-cadherin, β-catenin, and plakoglobin, and reduced the ICAM-1–mediated phosphorylation of VE-cadherin by immunofluorescence and confocal analysis and Western blot analysis, respectively. These findings indicate that α2-adrenoceptors trigger signals that protect the integrity of endothelial adherens junctions during the inflammatory response, thus pointing at the vascular endothelium as a therapeutic target for the management of inflammatory processes in humans.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Prevention of Neutrophil Extravasation by α2-Adrenoceptor–Mediated Endothelial Stabilization

Herrera-García

Domínguez-Luis

Arce-Franco

et al. 2014

The Journal of Immunology

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“…While there do not appear to be reports describing the presence of α adrenergic receptors on neutrophils in rodents (Altenburg et al, 1997;Madden et al, 1995), α 2 -adrenergic receptors do appear to exist in low abundance on human neutrophils (Varani et al, 2002). Furthermore, in several species, including mice, other blood cells, notably platelets (Hamilton et al, 1986;Maes et al, 2002;Mishra et al, 1985), macrophages (Garcia et al, 2003;Ignatowski et al, 2000;Javierre et al, 1975;Miles et al, 1996) and lymphocytes (Amenta et al, 2002;Felsner et al, 1995;Veglio et al, 2001), appear to either express α adrenergic receptors or respond to direct action by α-adrenergic receptor agonists. While α-adrenergic receptor agonists may affect neutrophil mobilization, it has been hypothesized that this is due to an indirect effect of α-adrenergic receptor stimulation on lymphocytes to release proinflammatory factors such as TNFα which then act on neutrophils and other cells (Altenburg et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

Coupade¹,

Brown²,

Dazin

et al. 2007

Journal of Neuroimmunology

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In wild-type FVB mice, leukocyte recruitment to lipopolysaccharide was sexually dimorphic, with a greater number of leukocytes recruited in females. In male β 2 -adrenergic receptor knock out mice (bred on a congenic FVB background) the number leukocytes recruited was increased ~4-fold, while in females there was no change, eliminating sexual dimorphism in leukocyte migration. While there were significantly fewer recruited CD62L + and CD11a + leukocytes in wild-type males, only in male β 2 -adrenergic receptor knock out mice was there an increase in the number of recruited CD11a + leukocytes, again eliminating sexual dimorphism. Thus, leukocyte migration and CD11a + adhesion molecule expression in male, but not in female, leukocytes is β 2 -adrenergic receptor-dependent. Our findings provide support for a role of β 2 -adrenergic receptor mechanisms in the inflammatory response, and suggest that β 2 -adrenergic receptor on male leukocytes contributes to sexual dimorphism in the effect of stress on inflammatory diseases.

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“…Few studies have revealed an effect of α-AR stimulation on B lymphocyte function [13,143,[239][240][241][242][243][244]. α 1 -or α 2 -AR stimulation increases or decreases in vitro T-dependent IgM production, respectively [13,143].…”

Section: Functional Significance Of Sympathetic Innervation Of Secondmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

226

185

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Optimal host defense against pathogens requires cross-talk between the nervous and immune systems. This paper reviews sympathetic-immune interaction, one major communication pathway, and its importance for health and disease. Sympathetic innervation of primary and secondary immune organs is described, as well as evidence for neurotransmission with cells of the immune system as targets. Most research thus far as focused on neural-immune modulation in secondary lymphoid organs, and have revealed complex sympathetic modulation resulting in both potentiation and inhibition of immune functions. SNS-immune interaction may enhance immune readiness during disease-or injury-induced 'fight' responses. Research also indicate that dysregulation of the SNS can significantly affect the progression of immune-mediated diseases. However, a better understanding of neural-immune interactions is needed to develop strategies for treatment of immune-mediated diseases that are designed to return homeostasis and restore normal functioning neural-immune networks.

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Adrenergic suppression of peripheral blood T cell reactivity in the rat is due to activation of peripheral α2-receptors

Cited by 60 publications

References 35 publications

Prevention of Neutrophil Extravasation by α2-Adrenoceptor–Mediated Endothelial Stabilization

Prevention of Neutrophil Extravasation by α2-Adrenoceptor–Mediated Endothelial Stabilization

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

Sympathetic modulation of immunity: Relevance to disease

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