Norepinephrine stimulates lymphoid cell mobilization from the perfused rat spleen via β-adrenergic receptors

Rogausch, H; Rey, Adriana del; Oertel, Jörg; Besedovsky, Hugo O.

doi:10.1152/ajpregu.1999.276.3.r724

Cited by 25 publications

(22 citation statements)

References 30 publications

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“…Furthermore, coadministration of epinephrine that normally counteracts the cardiovascular suppression induced by propranolol augmented the effect of this drug on the survival and on cellular immune functions. In addition, it was demonstrated that a ß-adrenergic blockade with or without the concomitant administration of an ·-adrenergic agonist did not increase the vascular resistance of the spleen [26]. We therefore assume that the increased mortality after the ß-adrenergic blockade in our experiment was mainly due to the observed immunologic changes rather than the consequence of local or systemic cardiovascular changes.…”

Section: Discussionmentioning

confidence: 58%

Adrenergic Modulation of Survival and Cellular Immune Functions during Polymicrobial Sepsis

Oberbeck

Schmitz

Wilsenack

et al. 2004

Neuroimmunomodulation

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Objective: An immunomodulatory effect of epinephrine has been reported that is supposed to be mediated via β-adrenergic receptors. The effect of epinephrine and/or β-adrenergic blockade on cellular immune functions during systemic inflammation has not yet been investigated. Methods: Male NMRI mice were treated with either an infusion of epinephrine (0.05 mg/kg/h i.p.), administration of the nonselective β-adrenoceptor antagonist propranolol (0.5 mg/kg s.c.), or a combination of epinephrine and propranolol after induction of a polymicrobial sepsis by cecal ligation and puncture. Forty-eight hours thereafter survival and cellular immune functions (splenocyte proliferation, splenocyte apoptosis and cytokine release, distribution of leukocyte subsets) were determined. Results: Infusion of epinephrine did not affect lethality of septic mice but induced alterations of splenocyte apoptosis, splenocyte proliferation and IL-2 release and was associated with profound changes of circulating immune cell subpopulations. Treatment with propranolol augmented the epinephrine-induced increase of splenocyte apoptosis, did not affect the decrease of splenocyte proliferation and IL-2 release, augmented the release of IL-6 and antagonized the mobilization of natural killer cells observed in epinephrine-treated animals. Furthermore, these immunologic alterations were accompanied by a significant increase of sepsis-induced mortality. Coadministration of propranolol and epinephrine augmented the propranolol-induced changes of splenocyte apoptosis and IL-6 release and was associated with the highest mortality of septic mice. Conclusion: Epinephrine infusion modulated cellular immune functions during systemic inflammation without an impact on survival. A pharmacologic β-adrenergic blockade partly augmented the epinephrine-induced immune alterations and was associated with a pronounced increase of mortality. This effect was further augmented by a combination of epinephrine infusion and β-adrenergic blockade. These data indicate that adrenergic mechanisms modulate cellular immune functions and survival during sepsis, with these effects being mediated via α- and β-adrenergic pathways.

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Section: Discussionmentioning

confidence: 58%

Adrenergic Modulation of Survival and Cellular Immune Functions during Polymicrobial Sepsis

Oberbeck

Schmitz

Wilsenack

et al. 2004

Neuroimmunomodulation

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“…Infusion of catecholamines into the spleen increases leukocyte output by either β-or α-AR mediated mechanisms in the absence of changes in blood flow [273]. Besedovsky and colleagues [274] have demonstrated that sympathetic innervation of the spleen alters flow resistance to affect leukocyte output from the spleen. Collectively these studies support a role for the SNS in regulating the cell entry, retention, and release from lymphoid organs.…”

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

225

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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“…3). In particular, catecholamines induce elevation in the number of circulating lymphocytes both in humans (4) and mice (5). The global effect of b-agonists on immunity was mainly studied by chemically depleting natural catecholamine stocks using 6-hydroxydopamine, which results in increased innate immune responses against bacteria (6), increased adaptive immune responses against virus (7), and decreased immune responses against Gram-positive bacteria (7)(8)(9).…”

mentioning

confidence: 99%

β2-Adrenoreceptor Agonist Inhibits Antigen Cross-Presentation by Dendritic Cells

Hervé

Dubreil

Tardif

et al. 2013

The Journal of Immunology

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Despite widespread usage of β-adrenergic receptor (AR) agonists and antagonists in current clinical practice, our understanding of their interactions with the immune system is surprisingly sparse. Among the AR expressed by dendritic cells (DC), β2-AR can modify in vitro cytokine release upon stimulation. Because DC play a pivotal role in CD8+ T cell immune responses, we examined the effects of β2-AR stimulation on MHC class I exogenous peptide presentation and cross-presentation capacities. We demonstrate that β2-AR agonist-exposed mature DC display a reduced ability to cross-present protein Ags while retaining their exogenous peptide presentation capability. This effect is mediated through the nonclassical inhibitory G (Gαi/0) protein. Moreover, inhibition of cross-presentation is neither due to reduced costimulatory molecule expression nor Ag uptake, but rather to impaired phagosomal Ag degradation. We observed a crosstalk between the TLR4 and β2-AR transduction pathways at the NF-κB level. In vivo, β2-AR agonist treatment of mice inhibits Ag protein cross-presentation to CD8+ T cells but preserves their exogenous MHC class I peptide presentation capability. These findings may explain some side effects on the immune system associated with stress or β-agonist treatment and pave the way for the development of new immunomodulatory strategies.

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Norepinephrine stimulates lymphoid cell mobilization from the perfused rat spleen via β-adrenergic receptors

Cited by 25 publications

References 30 publications

Adrenergic Modulation of Survival and Cellular Immune Functions during Polymicrobial Sepsis

Adrenergic Modulation of Survival and Cellular Immune Functions during Polymicrobial Sepsis

Sympathetic modulation of immunity: Relevance to disease

β2-Adrenoreceptor Agonist Inhibits Antigen Cross-Presentation by Dendritic Cells

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