Differential modulation of innate immune response by epinephrine and estradiol

Margaryan, Sona; Hyusyan, Armenuhi; Martirosyan, Anush; Sargsian, Shushan; Manukyan, Gayane

doi:10.1515/hmbci-2016-0046

Cited by 14 publications

(19 citation statements)

References 41 publications

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“…Additionally, catecholamines can alter cytokine levels and expression of adhesion molecules. Exposure to adrenaline in vitro increases interleukin-8 (IL-8) expression and CD11b (alpha-M-integrin) levels in human neutrophils (4). Under LPS-induced inflammatory conditions the production of IL-1, IL-8, and CCL2 is reduced, indicating that regulation of cytokines and chemokines by adrenaline is highly dependent on the inflammatory milieu (4).…”

Section: Catecholaminesmentioning

confidence: 99%

“…in vitro studies showed that after incubation with catecholamines and glucocorticoids, human granulocytes detach more easily by reducing their stiffness (3). In the bloodstream, human neutrophils show increased levels of CD11b as well as IL-8 after stimulation with adrenaline (4). However, their adhesion and trafficking in vitro are reduced due to downregulation of endothelial adhesion molecules (5, 6).…”

Section: Introductionmentioning

confidence: 99%

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Control of Leukocyte Trafficking by Stress-Associated Hormones

Weber²,

2019

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Leukocyte migration is a crucial process in both homeostatic and inflammatory conditions. The spatiotemporal distribution of immune cells is balanced between processes of cellular mobilization into the bloodstream, their adhesion to vascular beds and trafficking into tissues. Systemic regulation of leukocyte mobility is achieved by different signals including neuronal and hormonal cues, of which the catecholamines and glucocorticoids have been most extensively studied. These hormones are often associated with a stress response, however they regulate immune cell trafficking also in steady state, with effects dependent upon cell type, location, time-of-day, concentration, and duration of signal. Systemic administration of catecholamines, such as the sympathetic neurotransmitters adrenaline and noradrenaline, increases neutrophil numbers in the bloodstream but has different effects on other leukocyte populations. In contrast, local, endogenous sympathetic tone has been shown to be crucial for dynamic daily changes in adhesion molecule expression in the bone marrow and skeletal muscle, acting as a key signal to the endothelium and stromal cells to regulate immune cell trafficking. Conversely, glucocorticoids are often reported as anti-inflammatory, although recent data shows a more complex role, particularly under steady-state conditions. Endogenous changes in circulating glucocorticoid concentration induce redistribution of cells and potentiate inflammatory responses, and in many paradigms glucocorticoid action is strongly influenced by time of day. In this review, we discuss the current knowledge of catecholamine and glucocorticoid regulation of leukocyte migration under homeostatic and stimulated conditions.

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Section: Catecholaminesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Control of Leukocyte Trafficking by Stress-Associated Hormones

Weber²,

2019

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“…Wahle et al [24] have suggested that β2 adrenoreceptors are the principal factors that mediate cytokine production by PBMC. According to Margaryan et al [13] exposure of non-stimulated whole blood cells to epinephrine showed a dose-dependent increase in IL-8 secretion, whereas LPS stimulated cells expressed a markedly decreased IL-8 and IL-1β production. Howe-…”

Section: Discussionmentioning

confidence: 98%

“…It is evident therefore that increased epinephrine secretion during stress, as in cases of infection and inflammation, will activate the adrenoreceptors on the immune cells and enable them to respond to invading pathogens [12]. Accordingly, exposure of whole blood cells to epinephrine modulated pro-inflammatory cytokine production [13]. In these cases, innate cells, such as specific CD4+CD25− regulatory lymphocytes expressing β2-adrenoceptors, might play a crucial role in inflammation and particularly in sepsis, since when exposed to epinephrine they may restrain the production of pro-inflammatory cytokines [2].…”

Section: Effect Of Epinephrine On Cell Proliferationmentioning

confidence: 99%

Untitled

2020

Int J Immunol Immunother

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Background: Epinephrine is one of the major hormones orchestrating numerous physiological responses of the organism exposed to acute or chronic stress. In those cases the plasma level of the hormone exceeds manifold the physiological values present in healthy resting individuals. Higher epinephrine concentrations affect the immune system and modulate macrophages immune responses. The purpose of the present work was to detect if physiological concentrations of epinephrine may alter the capacity of human peripheral blood mononuclear cells (PBMC) for cytokine production, without and following co-incubation with HT-29 cells from a human colon cancer cell line. Methods: PBMC were incubated for 24 hours with the following concentrations of epinephrine-0.025 ng/ml, 0.05 ng/ ml and 0.1 ng/ml added at 10 µl/ml culture medium. The secretion of TNFα, IL-1β, IL-6, IFNγ, IL-10, and IL-2 was detected using the ELISA method. In another set of experiments the production of the same cytokines was assessed following co-incubation of PBMC with HT-29 cells. Results: 24 hrs of incubation with epinephrine had no effect on PBMC proliferation rate, whereas that of HT-29 colon cancer cells was significantly reduced. While epinephrine caused increased secretion of IL-6 by non-stimulated PBMC, the production of TNFα, IL-1β, IFNγ, and IL-10 was not affected. Epinephrine exerted no effect on TNFα, IL-1β, IL-6 and IL-10 production induced by LPS and on the release of IL-2 by PBMC activated with PMA. However the production of IFNγ by PBMC stimulated with PMA was increased. The secretion of pro-inflammatory cytokines hereby tested by HT-29-stimulated PBMC was not affected upon incubation with epinephrine. On the other hand, IL-10 secretion by HT-29 stimulated PBMC was slightly reduced. Conclusions: While small, physiological doses of epinephrine slightly stimulated PBMC for IL-6 and IL-10 production, it appears that the capacity of the mononuclear cells for massive cytokine release could be stirred only with extensive amounts of hormone, even higher than those freed during acute and chronic stress as studies have indicated. Small doses of epinephrine do not alter the immune cross talk between PBMC and HT-29 colon cancer cells.

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“…In fact, epinephrine was found to induce dose-dependently Il-8 production in unstimulated cells, but at the same time it suppressed IL-1β, IL-8, and monocyte chemotactic protein (MCP)-1 secretion in cells stimulated with lPS. 56…”

Section: The Adrenal Gland Microenvironmentmentioning

confidence: 99%

The adrenal gland microenvironment in health, disease and during regeneration

Kanczkowski

Sue

Bornstein

2017

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The adrenal gland is a key component of the stress system in the human body. Multiple direct and paracrine interactions between different cell types and their progenitors take place within the adrenal gland microenvironment. These unique interactions are supported by high vascularization and the adrenal cortex extracellular matrix. Alterations in the adrenal gland microenvironment are known to influence the progression of several pathological conditions, such as obesity and sepsis, and to be influenced by these disorders. For example, it has been suggested that activation of immune-adrenal crosstalk during sepsis induces elevated adrenal glucocorticoid levels, whereas crosstalk between adrenocortical cells and sonic hedgehog responsive stem cells was found to contribute to the increased size of the adrenal cortex during obesity. By contrast to sepsis, where activation of adrenal glucocorticoid production has protective effects, chronic exposure to high levels of glucocorticoids induces adverse effects, typically manifested in patients with Cushing syndrome, such as increased body weight, dyslipidemia, glucose intolerance, and hypertension. Therefore, a better understanding of factors involved in the regulation of the adrenal gland microenvironment is crucial. This review highlights bidirectional interactions occurring between the adrenal gland microenvironment and systemic responses during obesity and sepsis. Furthermore, it presents and discusses recent advancements and challenges in attempts to restore or regenerate adrenal gland function, including the use of oxygenated immune-isolating devices.

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Differential modulation of innate immune response by epinephrine and estradiol

Cited by 14 publications

References 41 publications

Control of Leukocyte Trafficking by Stress-Associated Hormones

Control of Leukocyte Trafficking by Stress-Associated Hormones

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The adrenal gland microenvironment in health, disease and during regeneration

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