Adrenergic modulation of migration, CD11b and CD18 expression, ROS and interleukin-8 production by human polymorphonuclear leukocytes

Scanzano, Angela; Schembri, Laura; Rasini, Emanuela; Luini, Alessandra; Dallatorre, Jessica; Legnaro, Massimiliano; Bombelli, R; Congiu, Terenzio; Cosentino, Marco; Marino, Franca

doi:10.1007/s00011-014-0791-8

Cited by 49 publications

(78 citation statements)

References 29 publications

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“…In particular, the inflammatory response of neutrophils involves the de novo production and release by these cells of catecholamines1213. Induced catecholamine stress (as during ischaemia) alters neutrophil trafficking141516 and promotes formation of neutrophil–platelet co-aggregates17.…”

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confidence: 99%

Neutrophil stunning by metoprolol reduces infarct size

et al. 2017

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The β1-adrenergic-receptor (ADRB1) antagonist metoprolol reduces infarct size in acute myocardial infarction (AMI) patients. The prevailing view has been that metoprolol acts mainly on cardiomyocytes. Here, we demonstrate that metoprolol reduces reperfusion injury by targeting the haematopoietic compartment. Metoprolol inhibits neutrophil migration in an ADRB1-dependent manner. Metoprolol acts during early phases of neutrophil recruitment by impairing structural and functional rearrangements needed for productive engagement of circulating platelets, resulting in erratic intravascular dynamics and blunted inflammation. Depletion of neutrophils, ablation of Adrb1 in haematopoietic cells, or blockade of PSGL-1, the receptor involved in neutrophil–platelet interactions, fully abrogated metoprolol's infarct-limiting effects. The association between neutrophil count and microvascular obstruction is abolished in metoprolol-treated AMI patients. Metoprolol inhibits neutrophil–platelet interactions in AMI patients by targeting neutrophils. Identification of the relevant role of ADRB1 in haematopoietic cells during acute injury and the protective role upon its modulation offers potential for developing new therapeutic strategies.

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confidence: 99%

Neutrophil stunning by metoprolol reduces infarct size

et al. 2017

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“…We have previously shown that, during activation with pro‐inflammatory stimuli, human PMN undergo morphological and functional changes, including changes in AR expression . We have also shown that these changes are followed by increased production of chemokines, such as IL‐8, and increased generation of ROS .…”

Section: Introductionmentioning

confidence: 88%

“…Experiments were performed on buffy coats of healthy subjects obtained by the local blood bank (Circolo Hospital, Fondazione Macchi, Varese, Italy). PMN were isolated by standard density‐gradient centrifugation as previously described . Cells were examined using light microscopy in order to exclude the presence of platelets or erythrocytes.…”

Section: Methodsmentioning

confidence: 99%

“…We have also shown that these changes are followed by increased production of chemokines, such as IL‐8, and increased generation of ROS . Finally, we have shown that these functional and morphological changes can be prevented by pharmacological treatments and involve the activation of specific AR‐operated pathways …”

Section: Introductionmentioning

confidence: 99%

“…TH is also expressed in immune cells, where it subserves endogenous production of CA, which in turn affect immune cell functions . CA can modulate hematopoiesis and their content in immune cells is affected by several diseases; cells of acquired and innate immunity express both adrenergic receptors (AR) and dopaminergic receptors (DR) and it has been shown that the activation of these receptors results in changes of different cell functions . Several studies have shown that these receptors are involved in immune‐mediated diseases …”

Section: Introductionmentioning

confidence: 99%

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β2-Adrenoceptors inhibit neutrophil extracellular traps in human polymorphonuclear leukocytes

Marino

Scanzano

Pulze

et al. 2018

Journal of Leukocyte Biology

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This study tests the hypothesis that in isolated human polymorphonuclear leukocytes (PMN) adrenergic ligands can affect neutrophil extracellular trap (NET) formation. We have previously shown that, in PMN, adrenaline (A), through the activation of adrenergic receptors (AR), reduces stimulus-dependent cell activation; we have, therefore, planned to investigate if AR are involved in NET production. PMN were obtained from venous blood of healthy subject. The ability of adrenergic ligands to affect reactive oxygen species (ROS) production, NET production, and cell migration was investigated in cells cultured under resting conditions or after activation with N-formyl-methionyl-leucyl-phenylalanine (fMLP), LPS, or IL-8. Stimuli-induced NET production measured as ROS, microscopic evaluation, and elastase production was reverted by A and this effect was blocked by the selective β -AR antagonist ICI-118,551. The stimulus-induced ROS generation and migration was prevented by A and by isoprenaline (ISO), and these effects were counteracted only by ICI-118,551 and not by the other two selective ligands for the β and β -AR. Finally, the presence of the β-ARs on PMN was confirmed, by means of microscopy and flow cytometry. The data of the present study suggest that adrenergic compounds, through the interaction of mainly β -AR, are able to affect neutrophil functions. These data are suggestive of a possible therapeutic role of β -AR ligands (in addition to their classical use), promoting the possible therapeutic relevance of adrenergic system in the modulation of innate immunity proposing their possible use as anti-inflammatory drugs.

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Chronic restraint stress promotes the mobilization and recruitment of myeloid‐derived suppressor cells through β‐adrenergic‐activated CXCL5‐CXCR2‐Erk signaling cascades

Cao

Huang

Chen

et al. 2021

Intl Journal of Cancer

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Myeloid-derived suppressor cells (MDSCs) play an important role in tumor immune escape. Recent studies have shown that MDSCs contribute to tumor progression under psychological stress, but the underlying mechanism of MDSCs mobilization and recruitment remains largely unknown. In the present study, a chronic restraint stress paradigm was applied to the H22 hepatocellular carcinoma (HCC) bearing mice to mimic the psychological stress. We observed that chronic restraint stress significantly promoted HCC growth, as well as the mobilization of MDSCs to spleen and tumor sites from bone marrow. Meanwhile, chronic restraint stress enhanced the expression of C-X-C motif chemokine receptor 2 (CXCR2) and pErk1/2 in bone marrow MDSCs, together with elevated chemokine (C-X-C motif) ligand 5 (CXCL5) expression in tumor tissues. In vitro, the treatments of MDSCs with epinephrine (EPI) and norepinephrine (NE) but not corticosterone (CORT)-treated H22 conditioned medium obviously inhibited T-cell proliferation, as well as enhanced CXCR2 expression and extracellular signal-regulated kinase (Erk) phosphorylation. In vivo, β-adrenergic blockade with propranolol almost completely reversed the accelerated tumor growth induced by chronic restraint stress and inactivated CXCL5-CXCR2-Erk signaling pathway. Our findings support the crucial role of β-adrenergic signaling cascade in the mobilization and recruitment of MDSCs under chronic restraint stress.

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Adrenergic modulation of migration, CD11b and CD18 expression, ROS and interleukin-8 production by human polymorphonuclear leukocytes

Abstract: Adrenergic agents reduced PMN responses mainly through β-AR, although α-AR may contribute at least to CD11b expression. AR-operated pathways in PMN should be investigated in disease conditions and in the response to therapeutic agents.

Cited by 49 publications

References 29 publications

Neutrophil stunning by metoprolol reduces infarct size

Neutrophil stunning by metoprolol reduces infarct size

β2-Adrenoceptors inhibit neutrophil extracellular traps in human polymorphonuclear leukocytes

Chronic restraint stress promotes the mobilization and recruitment of myeloid‐derived suppressor cells through β‐adrenergic‐activated CXCL5‐CXCR2‐Erk signaling cascades

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