Nerve Driven Immunity: Noradrenaline and Adrenaline

Cosentino, Marco; Marino, Franca

doi:10.1007/978-3-7091-0888-8_2

Cited by 8 publications

(4 citation statements)

References 268 publications

(262 reference statements)

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“…Considering that propranolol and glucocorticoids may affect catecholamine synthesis (Tuross & Patrick, 1986; Kvetnansky et al 2009; Cosentino & Marino, 2012), peritoneal exudate cells and/or macrophages were examined for noradrenaline content and the expression of enzymes involved in catecholamine metabolism.…”

Section: Resultsmentioning

confidence: 99%

“…In many cell types, glucocorticoids have been shown to modulate the expression of enzymes involved in both catecholamine biosynthesis and degradation. Specifically, they influence the expression of tyrosine hydroxylase (TH), the key enzyme in catecholamine biosynthesis, and monoamine oxidase‐A (MAO‐A), the major enzyme involved in catecholamine degradation in macrophages and lymphocytes (Kvetnansky et al 2009; Cosentino & Marino, 2012). In addition, it has been demonstrated that glucocorticoids affect the expression of both β‐ and α 1 ‐adrenoceptors (Wolfe et al 1976; Day et al 1999).…”

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confidence: 99%

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Adrenal hormone deprivation affects macrophage catecholamine metabolism and β₂‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

Stanojević

Dimitrijević

Kuštrimović

et al. 2013

Experimental Physiology

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New Findings r What is the central question of this study?Glucocorticoids modulate extraglandular catecholamine metabolism and adrenoceptor expression in many cell types. Catecholamines modulate the production of inflammatory mediators by macrophages. It was hypothesized that adrenal hormones affect tumour necrosis factor-α production in rat macrophages by altering the autocrine/paracrine action of catecholamines. r What is the main finding and its importance?In rat macrophages, adrenalectomy increased tyrosine hydroxylase expression, decreased monoamine oxidase-A mRNA expression (due to the absence of adrenal catecholamines and glucocorticoids, respectively) and augmented β 2 -adrenoceptor expression (due to lack of adrenal catecholamines). However, notwithstanding these changes, propranolol treatment increased lipopolysaccharide-stimulated tumour necrosis factor-α production in macrophages from adrenalectomized and non-operated rats to a similar extent.Catecholamines modulate the production of inflammatory mediators by macrophages in an autocrine/paracrine manner. They also tune β 2 -adrenoceptor expression. Glucocorticoids influence catecholamine metabolism and adrenoceptor expression in many cell types. We hypothesized that adrenal hormones affect the production of tumour necrosis factor-α (TNF-α) and NO by macrophages by altering the modulatory influence of catecholamines. To prove the hypothesis, peritoneal exudate macrophages from propranolol-treated nonoperated and adrenalectomized rats and from corticosterone-supplemented adrenalectomized rats were examined for lipopolysaccharide-stimulated NO and TNF-α production in vitro and for expression of β 2 -adrenoceptors and major catecholamine-metabolizing enzymes. Glucocorticoid deprivation increased NO production by macrophages, whereas 4 days of propranolol treatment was ineffective in this respect. However, propranolol treatment, via β 2 -adrenoceptor blockade, increased production of TNF-α by macrophages in both nonoperated and adrenalectomized rats (showing dramatically enhanced TNF-α production due to a lack of circulating glucocorticoids) for the same value. The expression of β 2 -adrenoceptor was increased in peritoneal macrophages that were freshly isolated from non-operated, propranolol-treated and adrenalectomized rats (due to adrenal catecholamine deficiency). Propranolol did not affect macrophage β 2 -adrenoceptor expression in adrenalectomized rats.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Adrenal hormone deprivation affects macrophage catecholamine metabolism and β₂‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

Stanojević

Dimitrijević

Kuštrimović

et al. 2013

Experimental Physiology

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“…Besedovsky and Del Rey [4] have suggested that, in addition to the affected cell subpopulation, the effects of NA also depend on the stimulus that triggers the immune response and, above all, on the activation stage at which macrophages and lymphocytes are exposed to neurotransmitters [5]. The processes directly or indirectly affected by sympathetic neurotransmitters are mainly the phagocytic process and antigenic presentation, the expression of adhesion molecules, the activation of lymphoid cells, the production of cytokines and chemokines, the Th1/Th2 balance, and the generation of cytotoxic cells [4,6,[8][9][10][11]. NA can also play a very important role in recirculation and leukocyte trafficking between lymphoid organs and blood [1,4,9,11], modulating chemotactic capacity and accumulation of phagocytes in inflammation sites as well [8,12,13].…”

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confidence: 99%

Adrenergic Regulation of Macrophage-Mediated Innate/Inflammatory Responses in Obesity and Exercise in this Condition: Role of β2 Adrenergic Receptors

Ortega

Gálvez

Martín-Cordero

2019

EMIDDT

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Background: The effects of exercise on the innate/inflammatory immune responses are crucially mediated by catecholamines and adrenoreceptors; and mediations in both stimulatory and anti-inflammatory responses have been attributed to them. Obesity and metabolic syndrome are included among low-grade chronic inflammatory pathologies; particularly because patients have a dysregulation of the inflammatory and stress responses, which can lead to high levels of inflammatory cytokines that induce insulin resistance, contributing to the onset or exacerbation of type 2 diabetes. Macrophages play a crucial role in this obesity-induced inflammation. Although most of the antiinflammatory effects of catecholamines are mediated by β adrenergic receptors (particularly β2), it is not known whether in altered homeostatic conditions, such as obesity and during exercise, innate/ inflammatory responses of macrophages to β2 adrenergic stimulation are similar to those in cells of healthy organisms at baseline. Objective: This review aims to emphasize that there could be possible different responses to β2 adrenergic stimulation in obesity, and exercise in this condition. Methods: A revision of the literature based on the hypothesis that obesity affects β2 adrenergic regulation of macrophage-mediated innate/inflammatory responses, as well as the effect of exercise in this context. Conclusion: The inflammatory responses mediated by β2 adrenoreceptors are different in obese individuals with altered inflammatory states at baseline compared to healthy individuals, and exercise can also interfere with these responses. Nevertheless, it is clearly necessary to develop more studies that contribute to widening the knowledge of the neuroimmune regulation process in obesity, particularly in this context.

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“…Increasing evidence indicates that DA plays an important role not only in mediating cross-talk between central nervous and immune systems , but also at a peripheral level by acting on tumor-associated immunologic alterations . Indeed, DA is synthesized, with rare exceptions, in most types of immune cells and released to the extracellular environment after specific stimulation . Due to the increasing interest in the use of immunotherapy as an efficient tool to boost the occurrence of the abscopal effect , and because of the DA interference with the immune system, a study of dopaminergic cell response to X-ray irradiation is necessary, especially in view of the potential synergy that it could have along with immunotherapy for malignant tumor treatment.…”

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confidence: 99%

Triggering Neurotransmitters Secretion from Single Cells by X-ray Nanobeam Irradiation

Picollo¹,

Tomagra

Bonino³

et al. 2020

Nano Lett.

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The employment of ionizing radiation is a powerful tool in cancer therapy, but beyond targeted effects, many studies have highlighted the relevance of its off-target consequences. An exhaustive understanding of the mechanisms underlying these effects is still missing, and no real-time data about signals released by cells during irradiation are presently available. We employed a synchrotron X-ray nanobeam to perform the first real-time simultaneous measurement of both X-ray irradiation and in vitro neurotransmitter release from individual adrenal phaeochromocytoma (PC12) cells plated over a diamond-based multielectrode array. We have demonstrated that, in specific conditions, X-rays can alter cell activity by promoting dopamine exocytosis, and such an effect is potentially very attractive for a more effective treatment of tumors.

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Nerve Driven Immunity: Noradrenaline and Adrenaline

Cited by 8 publications

References 268 publications

Adrenal hormone deprivation affects macrophage catecholamine metabolism and β₂‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

Adrenal hormone deprivation affects macrophage catecholamine metabolism and β₂‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

Adrenergic Regulation of Macrophage-Mediated Innate/Inflammatory Responses in Obesity and Exercise in this Condition: Role of β2 Adrenergic Receptors

Triggering Neurotransmitters Secretion from Single Cells by X-ray Nanobeam Irradiation

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Nerve Driven Immunity: Noradrenaline and Adrenaline

Cited by 8 publications

References 268 publications

Adrenal hormone deprivation affects macrophage catecholamine metabolism and β2‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

Adrenal hormone deprivation affects macrophage catecholamine metabolism and β2‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

Adrenergic Regulation of Macrophage-Mediated Innate/Inflammatory Responses in Obesity and Exercise in this Condition: Role of β2 Adrenergic Receptors

Triggering Neurotransmitters Secretion from Single Cells by X-ray Nanobeam Irradiation

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Adrenal hormone deprivation affects macrophage catecholamine metabolism and β₂‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production

Adrenal hormone deprivation affects macrophage catecholamine metabolism and β₂‐adrenoceptor density, but not propranolol stimulation of tumour necrosis factor‐α production