Expression of Granulocyte/Macrophage-Colony-Stimulating Factor, lnterleukin-8 and RANTES in the Bronchial Epithelium of Mild Asthmatics Is Down-Regulated by Inhaled Beclomethasone Dipropionate

Davies, Robert J.; Wang, Jia Hua; Trigg, C.J.; Devalia, Jagdish L.

doi:10.1159/000237068

Cited by 35 publications

(17 citation statements)

References 2 publications

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“…In particular, a correlation between therapeutic efficacy of inhaled corticosteroids and the decrease in the number of DC populating the bronchial mucosa of atopic asthmatic patients has been established, confirming the involvement of DC in asthmatic immune inflammation (10). Thus it seems reasonable to propose epithelial cells as a major target of glucocorticoid activity, since these drugs downregulate the expression of signals implicated in the local attraction and activation of a variety of inflammatory cells (48,49).…”

Section: Discussionmentioning

confidence: 72%

Granulocyte macrophage colony-stimulating factor is overproduced by keratinocytes in atopic dermatitis. Implications for sustained dendritic cell activation in the skin.

et al. 1997

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Lesional skin of atopic dermatitis (AD) harbors high numbers of dendritic cells with enhanced stimulatory capacity for T lymphocytes. In this study, lesional AD skin was shown to stain heavily in both epidermal and dermal compartments for GM-CSF, a cytokine crucial to dendritic cell functions. Keratinocyte cultures established from uninvolved skin of AD patients exhibited markedly increased spontaneous and PMA-stimulated release of GM-CSF compared with keratinocytes from nonatopic controls. Correspondingly, keratinocytes from AD patients showed higher constitutive as well as PMA-induced GM-CSF gene expression. Larger amounts of GM-CSF were produced by AD keratinocytes, also in response to IL-1 ␣ , but not after stimulation with LPS, lipoteichoic acid, or staphylococcal enterotoxin B. Hydrocortisone reduced GM-CSF gene expression and protein release in both atopic and control keratinocytes. Supernatants from atopic keratinocytes were able to strongly stimulate PBMC proliferation in a GM-CSF-dependent manner. Moreover, conditioned medium from PMA-treated AD keratinocytes, together with exogenous IL-4, could support phenotypical and functional maturation of peripheral blood precursors into dendritic cells. Enhanced production of GM-CSF by keratinocytes may contribute relevantly to the establishment and chronicity of AD lesions, in particular to the increased number, sustained activation, and enhanced antigen-presenting functions of dendritic cells. ( J. Clin. Invest. 1997. 99:3009-3017.)

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Section: Discussionmentioning

confidence: 72%

Granulocyte macrophage colony-stimulating factor is overproduced by keratinocytes in atopic dermatitis. Implications for sustained dendritic cell activation in the skin.

et al. 1997

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“…Human nasal and bronchial epithelial cells are capable of synthesising a wide number of cytokines, including IL-1, IL-3, IL-6, IL-8, GM-CSF, RANTES and TNF-α, monocyte chemoattractant protein (MCP)-1, GRO-α and GRO-γ, which possess potent proinflammatory actions (Raeburn and Webber, 1994 ;Levine, 1995). This cytokine production is upregulated in epithelial cells from those with allergic respiratory and nasal disorders (Raeburn and Webber, 1994 ;Levine, 1995 ;Devalia and Davies, 1993) and may be reduced by anti-allergic therapy (Kwon et al, 1995 ;Davies et al, 1995 ;Devalia et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

The Role of Conjunctival Epithelial Cells in Chronic Ocular Allergic Disease

Hingorani

Calder²,

Buckley

et al. 1998

Experimental Eye Research

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“…Diverse proinflammatory actions of RANTES include activation of eosinophils and T cells [4,5], adhesion of T cells to activated endothelium [6], and release of histamine from basophils [7]. Since RANTES is present at high levels in association with eosinophil-rich infiltrate in nasal polyps [8] and the bronchial epithelium of mild asthmatics [9], both clinical and biochemical data support a potentially critical role for RANTES in allergic inflammation.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoid‐mediated inhibition of RANTES expression in human T lymphocytes

Wingett¹,

Forcier²,

Nielson³

1996

FEBS Letters

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The ehemokine RANTES has been implicated in the pathogenesis of allergic inflammatory diseases including asthma and rhinitis which are frequently treated with glucocorticoids. We observed that dexamethasone dramatically inhibited RANTES mRNA expression dose dependently in anti-CD3 activated Hut-78 T cells and human PBMCs. Inhibition of RANTES expression did not appear to be secondary to IL-2 inhibition and required binding to the intracellular glucocorticoid receptor. The down-regulation of RANTES expression by glucocorticoids in T cells may directly contribute to the efficacy of these agents in suppressing cellular infiltration and to their anti-inflammatory properties.

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Expression of Granulocyte/Macrophage-Colony-Stimulating Factor, lnterleukin-8 and RANTES in the Bronchial Epithelium of Mild Asthmatics Is Down-Regulated by Inhaled Beclomethasone Dipropionate

Cited by 35 publications

References 2 publications

Granulocyte macrophage colony-stimulating factor is overproduced by keratinocytes in atopic dermatitis. Implications for sustained dendritic cell activation in the skin.

Granulocyte macrophage colony-stimulating factor is overproduced by keratinocytes in atopic dermatitis. Implications for sustained dendritic cell activation in the skin.

The Role of Conjunctival Epithelial Cells in Chronic Ocular Allergic Disease

Glucocorticoid‐mediated inhibition of RANTES expression in human T lymphocytes

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