Effects of Salmeterol Xinafoate and Fluticasone Propionate on Immunological Activation of Human Cultured Mast Cells

Akabane, Hirotomo; Murata, Masayuki; Kubota, Masafumi; Takashima, Eiji; Tanaka, Hiroyuki; Inagaki, Nobuya; Horiba, Michiaki; Nagai, Hiroichi

doi:10.2332/allergolint.55.387

Cited by 11 publications

(10 citation statements)

References 38 publications

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“…However, in vitro studies have suggested that there are dose-dependent effects of fluticasone on the inhibition of IL-8 and other mediators released from various types of cells, including airway epithelial cells [24], smooth muscle cells [25] and fibroblasts [26]. A synergistic effect of SFP on the inhibition of mediator release has also been demonstrated [27][28][29][30].…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Dw¹,

Cw²,

Kc³

et al. 2009

Eur Respir J

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The anti-inflammatory effects of salmeterol/fluticasone (SFP), tiotropium/fluticasone (Tio+FP) and tiotropium (Tio) alone were investigated on the inflammatory cells and mediators in sputum induced from chronic obstructive pulmonary disease patients.Subjects were either newly diagnosed or had not taken any medication for 3 months prior to the study. Subjects (n599) were randomised (not double blinded) and received either SFP (100/ 1,000 mg daily), Tio+FP (18/1,000 mg daily) or Tio (18 mg daily) for 12 weeks. Induced sputum and serum C-reactive protein (CRP) were analysed prior to and at the end of treatment.The results showed that treatment with SFP caused a significant reduction in interleukin (IL)-8 and matrix metalloprotease (MMP)-9 in induced sputum, compared with treatment with Tio alone. There were no treatment differences between the SFP and Tio+FP groups in decreasing IL-8 and MMP-9 levels. The reduction in IL-8 showed significant association with the reduction in MMP-9. All treatment groups failed to significantly reduce the numbers of total cells, neutrophils, macrophages and eosinophils in induced sputum; in addition, there were no treatment differences in terms of improvement of forced expiratory volume in one second, forced vital capacity, CRP or quality of life between the three groups.The anti-inflammatory effects of salmeterol/fluticasone probably contribute to the clinical benefits seen in chronic obstructive pulmonary disease patients.

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Section: Discussionmentioning

confidence: 99%

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Dw¹,

Cw²,

Kc³

et al. 2009

Eur Respir J

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“…Our previous studies have demonstrated that the rapid nongenomic effect of GCs functions by preventing the airway constriction reaction and inhibiting degranulation of mast cells in an allergic asthmatic model of guinea pigs (Zhou et al, 2008(Zhou et al, , 2003. In addition, GCs also have a potent inhibitory effect on cytokine release from a human mast cell line (Lippert et al, 1996;Akabane et al, 2006). It has been established that GCs affect β 2 -receptor-mediated signal transduction (Collins et al, 1988); the β 2 -receptor gene is responsive to transcriptional upregulation in response to GC exposure (Baraniuk et al, 1997).…”

Section: Introductionmentioning

confidence: 97%

Formoterol synergy with des-ciclesonide inhibits IL-4 expression in IgE/antigen-induced mast cells by inhibiting JNK activation

Sun

Jiang

et al. 2015

European Journal of Pharmacology

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“…Both short-acting β 2 -agonists, such as salbutamol and terbutaline, and longer-acting agonists such as salmeterol and formoterol, have also been demonstrated to inhibit the FcεRI-mediated degranulation and the release of PGD 2 , and LTs from human mast cells [96][97][98]. Moreover, β 2 agonists have been shown to inhibit IgE-dependent cytokine production such as GM-CSF and TNF-α in these cells [98,99]. As with other GPCRs that downregulate FcεRI-mediated degranulation, the inhibitory properties of β 2 agonists are mediated by the G sdependent activation of adenylate cyclase, and subsequent increase in intracellular cAMP [100].…”

Section: -Adrenergic Agonistsmentioning

confidence: 99%

“…β 2 -adrenoceptor agonists are used as bronchodilators in the therapeutic management of asthma [95,96]. Both short-acting β 2 -agonists, such as salbutamol and terbutaline, and longer-acting agonists such as salmeterol and formoterol, have also been demonstrated to inhibit the FcεRI-mediated degranulation and the release of PGD 2 , and LTs from human mast cells [96][97][98]. Moreover, β 2 agonists have been shown to inhibit IgE-dependent cytokine production such as GM-CSF and TNF-α in these cells [98,99].…”

mentioning

confidence: 99%

G protein-coupled receptors and the modification of FcɛRI-mediated mast cell activation

2007

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By releasing multiple pro-inflammatory mediators upon activation, mast cells are critical effector cells in the pathogenesis of allergic inflammation. The traditional viewpoint of antigen-dependent mast cell activation is that of a Th 2 -driven process whereby antigen-specific IgE molecules are produced by B cells followed by binding of the IgE to high affinity IgE receptors (FcεRI) expressed on mast cells. Subsequent antigen-dependent aggregation of the FcεRI initiates an intracellular signalling cascade that culminates in mediator release. Mast cell responses, including cell growth, survival, chemotaxis, and cell adhesion, however, can also be regulated by other receptors expressed on mast cells. Furthermore, FcεRI-mediated mast cell mediator release can be significantly modified by ligation of specific classes of these receptors. One such class of receptors is the G protein-coupled receptors (GPCR). In this review, we describe how sub-populations of GPCRs can either enhance or inhibit FcεRI-mediated mast cell activation depending on the particular G protein utilized for relaying signalling. Furthermore, we discuss the potential mechanisms whereby the signalling responses utilized by the FcεRI for mast cell activation are influenced by those initiated by GPCRs to produce these diverse responses. KeywordsMast cells; FcεRI; G protein-coupled receptors; IgE; antigen; signalling Mast cell activationMast cells play a role in both the innate and adaptive immune responses which contribute to the body's defence mechanisms against invading pathogens and parasites [1][2][3]. However, when mast cells are inappropriately activated following antigen exposure, the resulting release of multiple pro-inflammatory mediators leads to the initiation of the clinical manifestations associated with allergic inflammation [4]. This response occurs as a consequence of the antigen binding to IgE molecules which occupy high affinity receptors for IgE (FcεRI) on the mast cell surface and resulting cross-linking of these receptors [5,6]. FcεRI aggregation induces a cascade of intracellular signalling events which lead to the rapid release of histamine and proteolytic enzymes, as a consequence of degranulation, and the release of leukotrienes (LTs) and prostaglandins (PGs), as a result of phospholipase A 2 (PLA 2 )-mediated phospholipid hydrolysis [4,7]. Following enhanced gene expression, a variety of cytokines and chemokines * To whom correspondence be addressed: agilfillan@niaid.nih.gov, Bldg 10, Room 11C206, LAD, NIAID, NIH, 10 Center Drive, Bethesda, USA, MD 20892-1881, Phone: 301 496 8757, Fax: 301 480 8384. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the...

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Effects of Salmeterol Xinafoate and Fluticasone Propionate on Immunological Activation of Human Cultured Mast Cells

Abstract: The immunological release of chemical mediators (histamine, LT, PGD(2)) from HCMC was inhibited by SX but not by FP. SX and FP inhibited the production of GM-CSF by HCMC and both drug showed synergistic inhibition in the production of GM-CSF.

Cited by 11 publications

References 38 publications

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Anti-inflammatory effects of salmeterol/fluticasone, tiotropium/fluticasone or tiotropium in COPD

Formoterol synergy with des-ciclesonide inhibits IL-4 expression in IgE/antigen-induced mast cells by inhibiting JNK activation

G protein-coupled receptors and the modification of FcɛRI-mediated mast cell activation

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