Salmeterol, a β<sub>2</sub>-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice

Maris, Nico A.; Sluijs, Koenraad F. van der; Florquin, Sandrine; Vos, Alex F. de; Pater, Jennie M.; Jansen, Henk M.; Poll, Tom van der

doi:10.1152/ajplung.00125.2003

Cited by 42 publications

(45 citation statements)

References 42 publications

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“…The concept that ␤-adrenoceptor stimulation, whether it was endogenous or exogenous, can reduce lung endothelial permeability has been intermittently supported by a variety of experimental models (17,21,27,28) and one study in human volunteers (20), but the proof of its beneficial effect in an acute model of established severe bacterial pneumonia has not been previously demonstrated. ␤-Adrenoceptor stimulation may improve lung endothelial permeability (17,27,28) by inhibiting endothelial cell contraction and reducing intracellular gaps (19,34).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of endogenous β-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice

Su¹,

Robriquet²,

Folkesson³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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A. Matthay. Protective effect of endogenous ␤-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice. Am J Physiol Lung Cell Mol Physiol 290: L769 -L776, 2006. First published November 11, 2005 doi:10.1152/ajplung.00334.2005.-Some investigators have reported that endogenous ␤-adrenoceptor tone can provide protection against acute lung injury. Therefore, we tested the effects of ␤-adrenoceptor inhibition in mice with acute Escherichia coli pneumonia. Mice were pretreated with propranolol or saline and then intratracheally instilled with live E. coli (10 7 colony-forming units). Hemodynamics, arterial blood gases, plasma catecholamines, extravascular lung water, lung permeability to protein, bacterial counts, and alveolar fluid clearance were measured. Acute E. coli pneumonia was established after 4 h with histological evidence of acute pulmonary inflammation, arterial hypoxemia, a threefold increase in lung vascular permeability, and a 30% increase in extravascular lung water as an increase in plasma catecholamine levels. ␤-Adrenoceptor inhibition resulted in a marked increase in extravascular lung water that was explained by both an increase in lung vascular permeability and a reduction in net alveolar fluid clearance. The increase in extravascular lung water with propranolol pretreatment was not explained by an increase in systemic or vascular pressures. The increase in lung vascular permeability was explained in part by anti-inflammatory effects of ␤-adrenoceptor stimulation because plasma macrophage inflammatory protein-2 levels were higher in the propranolol pretreatment group compared with controls. The decrease in alveolar fluid clearance with propranolol was explained by a decrease in catecholamine-stimulated fluid clearance. Together, these results indicate that endogenous ␤-adrenoceptor tone has a protective effect in limiting accumulation of extravascular lung water in acute severe E. coli pneumonia in mice by two mechanisms: 1) reducing lung vascular injury and 2) upregulating the resolution of alveolar edema. Escherichia coli; alveolar fluid clearance; pulmonary edema; ␤-adrenoceptor inhibition; sodium channel EARLIER EXPERIMENTAL WORK established that elevated endogenous epinephrine levels can increase the capacity of the alveolar epithelium to remove alveolar edema fluid in the setting of septic or hemorrhagic shock (29,35,36) or after an acute neurogenic insult (18). However, the effects of endogenous ␤-adrenoceptor tone on lung fluid balance have not been studied in acute severe bacterial pneumonia, the most common cause of clinical acute lung injury (10). We would predict that an acute elevation in endogenous epinephrine and norepinephrine levels during acute bacterial pneumonia might elevate alveolar fluid clearance by cAMP-dependent mechanisms (3, 7, 8, 16, 22-24, 33, 37), providing the alveolar epithelial barrier has not been severely damaged by the bacteria or their products. Some investigations have suggested that endogenous ␤-adrenoceptor stimulation may downregulate ...

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Section: Discussionmentioning

confidence: 99%

Protective effect of endogenous β-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice

Su¹,

Robriquet²,

Folkesson³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…This response is rapidly tachyphylactic, reflecting the low density of b 2 -receptors on these cells. In animal models of neutrophilic inflammation, such as lipopolysaccharideinduced lung inflammation in mice, b-agonists have an inhibitory effect on neutrophil recruitment to the lung [48], which may be mediated by an inhibitory effect on the adhesion molecule CD11b on the cell surface [49]. Clinical studies have shown that in patients with mild asthma there is a decrease in neutrophils in bronchial biopsies and bronchoalveolar lavage after treatment with salmeterol, as well as a reduction in myeloperoxidase and human neutrophil lipocalin, indicating an inhibitory effect of neutrophil degranulation [50].…”

Section: Mast Cell Stabilisationmentioning

confidence: 99%

Scientific rationale for using a single inhaler for asthma control

Barnes¹

2007

Eur Respir J

139

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Clinical trials have recently demonstrated that using a budesonide/formoterol combination inhaler as regular maintenance treatment twice daily but also as a rescue therapy for breakthrough symptoms can provide more effective control of asthma, particularly in reducing exacerbations, than using a short-acting b 2 -agonist or formoterol as rescue therapy. This suggests that the corticosteroid component of the combination therapy plays an important role in rescue therapy.Formoterol as a rescue therapy is effective in relieving symptoms by relaxing airway smooth muscle but is also likely to have important inhibitory effects on mast cells, plasma exudation and neutrophilic inflammation.Inhaled corticosteroids have much more rapid suppressing effects on airway inflammation than previously recognised and the increased dose used as rescue therapy may prevent the increase in airway inflammation that occurs during the evolution of an exacerbation, thus preventing its development.It is likely that the molecular interactions between b 2 -agonists and corticosteroids also enhance the effect of the combination therapy as rescue therapy. There is now a strong scientific rationale for single inhaler therapy in asthma, but more research is now needed to better understand the mechanisms involved.

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“…In addition to bronchodilation, -agonists may also possess anti-inflammatory activity (Barnes, 2006;Theron et al, 2013). Both in vitro and in vivo studies suggest that -agonists may dampen inflammation although there are inconsistencies (Schild, 1937;O'Connor et al, 1994;Maris et al, 2004, Maris et al, 2005Bosmann et al, 2012;Wex et al, 2015). It is noteworthy that in many of these studies animal models or cell lines have been employed.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of the anti-inflammatory effects of β-adrenoceptor agonists on human lung macrophages

Gill

Marriott

Suvarna

et al. 2016

European Journal of Pharmacology

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Salmeterol, a β₂-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice

Abstract: der Poll. Salmeterol, a ␤2-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice.

Cited by 42 publications

References 42 publications

Protective effect of endogenous β-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice

Protective effect of endogenous β-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice

Scientific rationale for using a single inhaler for asthma control

Evaluation of the anti-inflammatory effects of β-adrenoceptor agonists on human lung macrophages

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Salmeterol, a β2-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice

Abstract: der Poll. Salmeterol, a ␤2-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice.

Cited by 42 publications

References 42 publications

Protective effect of endogenous β-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice

Protective effect of endogenous β-adrenergic tone on lung fluid balance in acute bacterial pneumonia in mice

Scientific rationale for using a single inhaler for asthma control

Evaluation of the anti-inflammatory effects of β-adrenoceptor agonists on human lung macrophages

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Salmeterol, a β₂-receptor agonist, attenuates lipopolysaccharide-induced lung inflammation in mice