Characterization of tolerance to the anti-leakage effect of formoterol in rat airways

Bowden, Jeffrey; Anderson, Gary P.; Lefevre, Peter; Sulakvelidze, I.; McDonald, Donald M.

doi:10.1016/s0014-2999(97)01272-7

Cited by 7 publications

(3 citation statements)

References 15 publications

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“…However, measurement of sputum a 2 -macroglobulin, a plasma marker, is significantly reduced by formoterol after histamineinduced increase in leakage in normal subjects [35], indicating that therapeutic doses of formoterol are able to inhibit plasma exudation. The anti-leakage effect of b 2 -agonists shows the development of tolerance when high doses are used, but it is not certain if this is prevented by corticosteroids [36].…”

Section: Reduced Plasma Exudationmentioning

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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Section: Reduced Plasma Exudationmentioning

confidence: 99%

Scientific rationale for using a single inhaler for asthma control

Barnes¹

2007

Eur Respir J

139

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“…LABAs inhibit neutrophil respiratory burst [35] and reduce adhesion of neutrophils to airway epithelial cells through inhibition of the expression of CD11b/CD18 on the neutrophil surface [36]. LABAs also reduce airway microvascular leakage, which is increased in COPD [37][38][39], all of which suggest an anti-inflammatory profile. There is also an increase in ciliary beating through an effect on epithelial b 2 -receptors, which may increase mucociliary clearance [40,41].…”

Section: Long-acting Bronchodilatorsmentioning

confidence: 99%

COPD: current therapeutic interventions and future approaches

Barnes¹

2005

Eur Respir J

233

143

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Although long-acting bronchodilators have been an important advance for the management of chronic obstructive pulmonary disease (COPD), these drugs do not deal with the underlying inflammatory process. No currently available treatments reduce the progression of COPD or suppress the inflammation in small airways and lung parenchyma. Several new treatments that target the inflammatory process are now in clinical development. Some therapies, such as chemokine antagonists, are directed against the influx of inflammatory cells into the airways and lung parenchyma that occurs in COPD, whereas others target inflammatory cytokines such as tumour necrosis factor-a.Broad spectrum anti-inflammatory drugs are now in phase III development for COPD, and include phosphodiesterase-4 inhibitors. Other drugs that inhibit cell signalling include inhibitors of p38 mitogen-activated protein kinase, nuclear factor-kB and phosphoinositide-3 kinase-c. More specific approaches are to give antioxidants, inhibitors of inducible nitric oxide synthase and leukotriene B 4 antagonists. Other treatments have the potential to combat mucus hypersecretion, and there is also a search for serine proteinase and matrix metalloproteinase inhibitors to prevent lung destruction and the development of emphysema.More research is needed to understand the cellular and molecular mechanisms of chronic obstructive pulmonary disease and to develop biomarkers and monitoring techniques to aid the development of new therapies.

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“…The dosage of drugs was chosen according to and slightly modified from previous studies for their effectiveness in similar applications. 5,32,63 Owing to the long-lasting act of formoterol, a single dose of formoterol was injected. A second dose of ICI118551 was injected on day 3 after colitis induction.…”

Section: Drug Treatmentmentioning

confidence: 99%

Beta 2-adrenergic receptor mediates noradrenergic action to induce cyclic adenosine monophosphate response element-binding protein phosphorylation in satellite glial cells of dorsal root ganglia to regulate visceral hypersensitivity

Shen

Tiwari

Madar

et al. 2021

Pain

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Sympathoneuronal outflow into dorsal root ganglia (DRG) is suggested to be involved in sympathetically maintained chronic pain, which is mediated by norepinephrine (NE) action on DRG cells. This study combined in vitro and in vivo approaches to identify the cell types of DRG that received NE action and examined cell type-specific expression of adrenergic receptors (ARs) in DRG. Using DRG explants, we identified that NE acted on satellite glial cells (SGCs) to induce the phosphorylation of cAMP response element-binding protein (CREB). Using primarily cultured SGCs, we identified that beta (b)2-adrenergic receptor but not alpha (a)adrenergic receptor nor other bAR isoforms mediated NE-induced CREB phosphorylation and CRE-promoted luciferase transcriptional activity. Using fluorescence in situ hybridization and affinity purification of mRNA from specific cell types, we identified that b2AR was expressed by SGCs but not DRG neurons. We further examined b2AR expression and CREB phosphorylation in vivo in a model of colitis in which sympathetic nerve sprouting in DRG was observed. We found that b2AR expression and CREB phosphorylation were increased in SGCs of thoracolumbar DRG on day 7 after colitis induction. Inhibition but not augmentation of b2AR reduced colitis-induced calcitonin generelated peptide release into the spinal cord dorsal horn and colonic pain responses to colorectal distention. Prolonged activation of b2AR in naive DRG increased calcitonin gene-related peptide expression in DRG neurons. These findings provide molecular basis of sympathetic modulation of sensory activity and chronic pain that involves b2AR-mediated signaling in SGCs of DRG.

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Characterization of tolerance to the anti-leakage effect of formoterol in rat airways

Cited by 7 publications

References 15 publications

Scientific rationale for using a single inhaler for asthma control

Scientific rationale for using a single inhaler for asthma control

COPD: current therapeutic interventions and future approaches

Beta 2-adrenergic receptor mediates noradrenergic action to induce cyclic adenosine monophosphate response element-binding protein phosphorylation in satellite glial cells of dorsal root ganglia to regulate visceral hypersensitivity

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