Anti-inflammatory effect of β-agonists: Inhibition of TNF-α release from human mast cells

Bissonnette, Élyse; Befus, A. Dean

doi:10.1016/s0091-6749(97)70280-x

Cited by 90 publications

(62 citation statements)

References 49 publications

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“…For example, addition of salbutamol to cultures of stimulated monocytes [35] or neutrophils [36] reduces their secretion of CXCL8/IL-8, although it increases or does not affect expression of this chemokine by transformed epithelial cells [23] or airway smooth muscle cells [37], respectively. Some b 2 -agonists can downregulate the expression by human mast cells [38] or eosinophils [39] of TNF or superoxide, respectively, and a single dose of salmeterol can inhibit allergen-induced changes in nasal mucosa vascular permeability, but does not reduce mast cell activation or cellular influx in vivo [40]. Conversely, prolonged in vitro exposure of eosinophils to b 2 -agonists increases cellular superoxide release [39].…”

Section: Discussionmentioning

confidence: 99%

Regular salbutamol use increases CXCL8 responses in asthma: relationship to the eosinophil response

Gordon

Swystun²,

Li³

et al. 2003

Eur Respir J

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Regular salbutamol use can exacerbate allergen-induced airway eosinophilia in asthmatics, but its effect on airway eosinophil chemokine responses is unknown.Asthmatic subjects (n=14) were treated for 10 days with placebo or salbutamol in a double-blind, cross-over study, then given same-dose allergen challenges. Their sputa were then analysed 1 and 7 h later for a panel of eosinophil-related cytokines. Eosinophils from five test and three control subjects were tested for expression of CXCL8/interleukin (IL)-8, and its receptors and responsiveness to CCL11/eotaxin and CXCL8/IL-8.Sputum CXCL8/IL-8, but not IL-5, CCL5/regulated on activation, T-cell expressed and secreted, CCL7/monocyte chemotactic protein-3, CCL11/eotaxin, granulocytemacrophage colony-stimulating factor or tumour necrosis factor levels, were increased (42%) by the salbutamol treatments. The CXCL8/IL-8 levels correlated with the proportions of sputum eosinophils and these cells, but not other sputum cells, stained strongly for CXCL8/IL-8. The circulating eosinophils of the tested subjects (n=5) expressed CXCL8/IL-8 receptors and secreted high levels of this chemokine. Neutralisation of sputum CXCL8/IL-8 reduced eosinophil chemotactic responses to these samples by 19¡5%.These data suggest that regular use of salbutamol can augment airway CXCL8/ interleukin-8 responses to allergen challenge and that this CXCL8/interleukin-8 could contribute to the airway inflammatory response. Eur Respir J 2003; 22: 118-126 Inhaled b 2 -adrenergic receptor agonists (b 2 -agonists) comprise a primary therapy for bronchoconstriction in allergic asthma patients. However, evidence suggests that regular use of b 2 -agonists can reduce their effectiveness [1, 2] and lead to increased airway hyperresponsiveness [3][4][5] and eosinophil/ mast cell responses [4,5] to allergen challenge. Given the association of eosinophils with asthma severity and pathology [6], the cellular mechanisms that may regulate this eosinophil response were questioned.Eosinophils express receptors for many molecules that are highly pertinent to asthma pathophysiology [6]. For example, the CCR3 receptor, which binds multiple CC chemokines (e.g. CCL11/eotaxin [6]), is broadly accepted as critical to the eosinophil response. However, CXCL8/interleukin (IL)-8 is also strongly expressed within allergic lesions [7][8][9][10] and eosinophils are responsive to this CXCR1/CXCR2 ligand [11,12]. Indeed, the decreased eosinophilia after allergen immunotherapy may be related to reduced CXCL8/IL-8 responses to allergen challenge [13].In a recent study in which mildly asthmatic subjects (n=14) regularly used salbutamol (or placebo) for 10 days, an exacerbation of asthmatic responses (forced expiratory volume in one second (FEV1), serum tryptase and sputum eosinophils) to allergen challenge was observed [5]. In order to gain insight into potential mechanisms behind this eosinophilia [4,5], a panel of nine pertinent eosinophil-signalling cytokines/ chemokines in sputum, previously obtained from these subjec...

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Section: Discussionmentioning

confidence: 99%

Regular salbutamol use increases CXCL8 responses in asthma: relationship to the eosinophil response

Gordon

Swystun²,

Li³

et al. 2003

Eur Respir J

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“…Although b 2 -agonists are commonly used as a bronchodilator, they also possess anti-in¯ammatory activities by inhibiting the release of in¯ammatory mediators (Erjefalt & Persson, 1991;Bissonnette & Befus, 1997). The inhibitory e ects of b 2 -agonists on TNF-a production have been reported in human blood, leukocytes and mast cells (Severn et al, 1992;Bissonnette & Befus, 1997). Our studies showed that both a non-selective b-agonist and a b 2 -selective agonist attenuate LPS-induced change in vascular permeability of mouse skin.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of cyclic AMP elevating agents on lipopolysaccharide (LPS)‐induced microvascular permeability change in mouse skin

Irie

Fujii

Ishida

et al. 2001

British J Pharmacology

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1 Anti-in¯ammatory e ects of cyclic AMP elevating agents were examined in a mouse model of lipopolysaccharide (LPS)-induced microvascular permeability change. 2 Vascular permeability on the back skin was measured by the local accumulation of Pontamine sky blue (PSB) after subcutaneous injection of LPS (400 mg site 71 ) from Salmonella typhimurium. 3 Dye leakage in the skin was signi®cantly increased 2 h after injection of LPS. This LPS-induced dye leakage was suppressed by phosphodiesterase inhibitors, including pentoxifylline (160 mg kg 71 ), milrinone (5 ± 10 mg kg 71 ), rolipram (0.5 ± 10 mg kg 71 ) and zaprinast (5 ± 10 mg kg 71 ). The dye leakage was also inhibited by b-adrenoceptor agonists, including isoproterenol (0.5 ± 5 mg kg 71 ) and salbutamol (0.05 ± 5 mg kg 71 ), an adenylate cyclase activator, forskolin (5 mg kg 71 ), and a cell permeable cyclic AMP analogue, 8-bromo-cyclic AMP (8-Br-cAMP, 10 mg kg 71 ). 4 LPS caused a transient increase in serum TNF-a level peaking at 1 h after the injection. This increase in serum TNF-a was completely blocked by a pretreatment with pentoxifylline (160 mg kg 71 ), milrinone (5 mg kg 71 ), rolipram (1 mg kg 71 ), zaprinast (10 mg kg 71 ), salbutamol (0.5 mg kg 71 ), forskolin (1 mg kg 71 ) and 8-Br-cAMP (10 mg kg 71 ). 5 LPS caused an increase in serum IL-1a level peaking at 3 h after injection. This increase in serum IL-1a was not signi®cantly suppressed by the cyclic AMP elevating agents. 6 Our study suggests that cyclic AMP elevating agents attenuate LPS-induced microvascular permeability change by suppressing TNF-a up regulation.

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“…␣-and ␤-〈Rs were detected in keratinocytes and melanocytes of human skin (219, 220, 715, 813, 814). Additionally, ␤-〈R agonists inhibited TNF-␣ release from mast cells (72) and are potent inhibitors of the IgE-mediated release of tryptase mediators from human mast cells in vitro (834). ␣-and ␤-〈Rs may also regulate important vascular responses in the skin such as vasoconstriction (215,319).…”

Section: Adrenergic Receptorsmentioning

confidence: 99%

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

Roosterman¹,

Goerge

Schneider

et al. 2006

Physiological Reviews

548

521

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This review focuses on the role of the peripheral nervous system in cutaneous biology and disease. During the last few years, a modern concept of an interactive network between cutaneous nerves, the neuroendocrine axis, and the immune system has been established. We learned that neurocutaneous interactions influence a variety of physiological and pathophysiological functions, including cell growth, immunity, inflammation, pruritus, and wound healing. This interaction is mediated by primary afferent as well as autonomic nerves, which release neuromediators and activate specific receptors on many target cells in the skin. A dense network of sensory nerves releases neuropeptides, thereby modulating inflammation, cell growth, and the immune responses in the skin. Neurotrophic factors, in addition to regulating nerve growth, participate in many properties of skin function. The skin expresses a variety of neurohormone receptors coupled to heterotrimeric G proteins that are tightly involved in skin homeostasis and inflammation. This neurohormone-receptor interaction is modulated by endopeptidases, which are able to terminate neuropeptide-induced inflammatory or immune responses. Neuronal proteinase-activated receptors or transient receptor potential ion channels are recently described receptors that may have been important in regulating neurogenic inflammation, pain, and pruritus. Together, a close multidirectional interaction between neuromediators, high-affinity receptors, and regulatory proteases is critically involved to maintain tissue integrity and regulate inflammatory responses in the skin. A deeper understanding of cutaneous neuroimmunoendocrinology may help to develop new strategies for the treatment of several skin diseases.

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Anti-inflammatory effect of β-agonists: Inhibition of TNF-α release from human mast cells

Cited by 90 publications

References 49 publications

Regular salbutamol use increases CXCL8 responses in asthma: relationship to the eosinophil response

Regular salbutamol use increases CXCL8 responses in asthma: relationship to the eosinophil response

Inhibitory effects of cyclic AMP elevating agents on lipopolysaccharide (LPS)‐induced microvascular permeability change in mouse skin

Neuronal Control of Skin Function: The Skin as a Neuroimmunoendocrine Organ

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