Rapid anti-secretory effects of glucocorticoids in human airway epithelium

Urbach, V.; Verrière, Valia; Grumbach, Y; Bousquet, Jean; Harvey, Bill

doi:10.1016/j.steroids.2005.09.014

Cited by 35 publications

(27 citation statements)

References 58 publications

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“…These effects were suppressed by inhibitors of adenylyl cyclase and PKA activity, and by blocking Ca 2+ release from intracellular stores. They also demonstrated a rapid, non-genomic glucocorticoid modulation of bronchial epithelial cell pH by stimulation of the Na + /H + exchanger, which was also mediated by a PKA-dependent pathway as well as mitogen-activated protein kinase (MAPK) and extracellular signalregulated kinase 1 and 2 (ERK 1 and ERK 2 ) activation (Urbach et al, 2006;Verriere et al, 2005). A glucocorticoid-activated, non-genomic pathway was also shown to block ATPevoked and P2X receptor-stimulated Ca 2+ influx in mouse HT4 neuroblastoma cells via a PKAdependent mechanism (Han et al, 2005).…”

Section: Non-genomic Action Of Glucocorticoids In the Hypothalamusmentioning

confidence: 99%

Glucocorticoids shift arachidonic acid metabolism toward endocannabinoid synthesis: A non-genomic anti-inflammatory switch

Malcher‐Lopes

Franco

Tasker

2008

European Journal of Pharmacology

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Glucocorticoids are capable of exerting both genomic and non-genomic actions in target cells of multiple tissues, including the brain, which trigger an array of electrophysiological, metabolic, secretory and inflammatory regulatory responses. Here, we have attempted to show how glucocorticoids may generate a rapid anti-inflammatory response by promoting arachidonic acidderived endocannabinoid biosynthesis. According to our hypothesized model, non-genomic action of glucocorticoids results in the global shift of membrane lipid metabolism, subverting metabolic pathways toward the synthesis of the anti-inflammatory endocannabinoids, anandamide (AEA) and 2-arachidonoyl-glycerol (2-AG), and away from arachidonic acid production. Post-transcriptional inhibition of cyclooxygenase-2 (COX 2 ) synthesis by glucocorticoids assists this mechanism by suppressing the synthesis of pro-inflammatory prostaglandins as well as endocannabinoid-derived prostanoids. In the central nervous system (CNS) this may represent a major neuroprotective system, which may cross-talk with leptin signaling in the hypothalamus allowing for the coordination between energy homeostasis and the inflammatory response.

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Section: Non-genomic Action Of Glucocorticoids In the Hypothalamusmentioning

confidence: 99%

Glucocorticoids shift arachidonic acid metabolism toward endocannabinoid synthesis: A non-genomic anti-inflammatory switch

Malcher‐Lopes

Franco

Tasker

2008

European Journal of Pharmacology

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“…A physical and functional interaction between the GR and the T-cell receptor (TCR) complex [9] and membrane-bound GR induced phosphorylation of p38 mitogen-activated protein kinase (MAPK) due to DEX/bovine serum albumin (BSA) treatment [10] has been reported. Low concentrations of DEX rapidly regulate intracellular pH, Ca 2+ and cAMP-dependent protein kinase activity, and inhibit Cl -secretion in bronchial epithelial cells via nongenomic mechanisms [11]. A recent study showed that inhaled fluticasone propionate (FP) and budesonide (BUD) stimulate cystic fibrosis transmembrane conductance regulator (CFTR)-mediated anion transport through adenylate cyclase-mediated mechanisms in a nongenomic fashion [12].…”

Section: Mechanisms Of Action Of Gcmentioning

confidence: 99%

Recent Topics in Steroid and Asthma: Beyond the 'Classic' Concept of Action

Matsumura¹

2015

Glob J Allergy

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SummaryGlucocorticoid (GC)s exert anti-inflammatory effects via binding to the glucocorticoid receptor (GR) (NR3C1), targeted gene expression, and protein synthesis, which need hours before the onset of the action (transactivation). GCs also suppress inflammation by direct or indirect interaction with transcription factors, such as activator protein-1 (AP-1) and nuclear factor-κB (NF-κB) (transrepression). Recently, the non-genomic actions of GCs were discovered on recognition of its rapid onset of action within seconds to minutes.GCs target many cells and tissues, including immune and inflammatory cells, airway epithelium, and airway smooth muscle (ASM). Of these, ASM is involved in altered airway contractility. A recent study demonstrated that GCs not only suppress inflammation but also exert direct effects on ASM gene expression which influence ASM function.GC resistance in the treatment of bronchial asthma remains a considerable clinical problem. Genes and cellular inflammatory phenotypes of glucocorticoid-resistant (GC-R) asthma have been revealed. Inflammation-associated protein kinase signaling and transcription factors affect GC actions through modulating GR function. Involvement of chromatin modifications have also been reported. Infection, reduced Vitamin D (Vit D), smoking, and obesity are preventable risk factors in GC-R asthma.Some of these recently available results are presented in this review.

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“…This connection inhibits gene transcription by direct binding to DNA or by inducing histone deacetylation. Although the non-genomic effect of GC is widely known in the literature [2,17], there is no report on its effect on chronic upper respiratory diseases, and only few studies have reported controversial results regarding asthma [40,41].…”

Section: Glucocorticoid Action On Nasal Mucosamentioning

confidence: 99%