Fluticasone, but not salmeterol, reduces cigarette smoke-induced production of interleukin-8 in human airway smooth muscle

Oltmanns, Ute; Walters, M. R.; Sukkar, Maria B.; Xie, Shaoping; Issa, Razao; Mitchell, Jane A.; Johnson, Malcolm; Chung, Kian Fan

doi:10.1016/j.pupt.2007.07.001

Cited by 17 publications

(15 citation statements)

References 38 publications

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“…In this context patients with COPD who smoke or who have stopped smoking are known to experience continuing oxidative stress 37 that might be associated with relative steroid resistance. 38,39 We showed that GSH significantly inhibited CSE-mediated IKKa and IKKb activity and that FP moderately but significantly improved its downregulatory effects on IKKa activity in the presence of GSH. These results suggest that the reduced ability of FP to inhibit IKKa and IKKb is sustained by unresolved oxidative stress and might in part explain the poor or absent response to glucocorticosteroids that characterizes COPD.…”

Section: Discussionmentioning

confidence: 89%

“…These results suggest that the reduced ability of FP to inhibit IKKa and IKKb is sustained by unresolved oxidative stress and might in part explain the poor or absent response to glucocorticosteroids that characterizes COPD. 39 In addition, the finding that the presence of GSH potentiates the effects of FP on IKKa and IKKb activity, generating a similar modulation of both kinases by glucocorticosteroids, suggests that targeting cigarette smokeinduced oxidative stress might have beneficial outcomes in the treatment of COPD. 40 IL-8 synthesis is highly NF-kB dependent, and this process requires both IKKa and IKKb activity.…”

Section: Discussionmentioning

confidence: 99%

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IκB kinase–driven nuclear factor-κB activation in patients with asthma and chronic obstructive pulmonary disease

Gagliardo¹,

Chanez²,

Profita³

et al. 2011

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

IκB kinase–driven nuclear factor-κB activation in patients with asthma and chronic obstructive pulmonary disease

Gagliardo¹,

Chanez²,

Profita³

et al. 2011

Journal of Allergy and Clinical Immunology

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“…CS has been shown to induce IL-8 release from ASM cells (10,30,31). This may involve oxidative stress, as the CSinduced IL-8 release was inhibited by glutathione pretreatment and associated with increased expression of heme oxygenase-1 (30).…”

Section: Discussionmentioning

confidence: 99%

“…risk factor of COPD, has been shown to induce the release of interleukin-8 (IL-8) from ASM cells, which positions these cells to contribute to increased neutrophil influx to the airways (10,30,31). The proportion of airways containing neutrophils, as well as other inflammatory cells, has been found to correlate with COPD severity (15).…”

mentioning

confidence: 99%

Role for TAK1 in cigarette smoke-induced proinflammatory signaling and IL-8 release by human airway smooth muscle cells

Pera

Atmaj

Vegt

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Chronic obstructive pulmonary disease (COPD) is an inflammatory disease, characterized by a progressive decline in lung function. Airway smooth muscle (ASM) mass may be increased in COPD, contributing to airflow limitation and proinflammatory cytokine production. Cigarette smoke (CS), the major risk factor of COPD, causes ASM cell proliferation, as well as interleukin-8 (IL-8)-induced neutrophilia. In various cell types, transforming growth factor-β-activated kinase 1 (TAK1) plays a crucial role in MAP kinase and NF-κB activation, as well as IL-8 release induced by IL-1β, TNF-α, and lipopolysaccharide. The role of TAK1 in CS-induced IL-8 release is not known. The aim of this study was to investigate the role of TAK1 in CS-induced NF-κB and MAP kinase signaling and IL-8 release by human ASM cells. Stimulation of these cells with CS extract (CSE) increased IL-8 release and ERK-1/2 phosphorylation, as well as Iκ-Bα degradation and p65 NF-κB subunit phosphorylation. CSE-induced ERK-1/2 phosphorylation and Iκ-Bα degradation were both inhibited by pretreatment with the specific TAK1 inhibitor LL-Z-1640-2 (5Z-7-oxozeaenol; 100 nM). Similarly, expression of dominant-negative TAK1 inhibited CSE-induced ERK-1/2 phosphorylation. In addition, inhibitors of TAK1 and the NF-κB (SC-514; 50 μM) and ERK-1/2 (U-0126; 3 μM) signaling inhibited the CSE-induced IL-8 release by ASM cells. These data indicate that TAK1 plays a major role in CSE-induced ERK-1/2 and NF-κB signaling and in IL-8 release by human ASM cells. Furthermore, they identify TAK1 as a novel target for the inhibition of CS-induced inflammatory responses involved in the development and progression of COPD.

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“…Also, in vitro studies have shown that airway smooth muscle cells produce IL-8 in response to many inflammatory mediators implicated in COPD, including TNF-a [42], IL-17 [43] and neutrophil products, such as LL-37 [44], bacteria [45] and cigarette smoke [18]. Combining cigarette smoke with TNF-a results in a synergistic increase in IL-8 release [46]. Our data also show that muscarinic receptor agonists can act in concert with cigarette smoke to induce the production of IL-8 by airway smooth muscle cells, suggesting that these cells, in addition to epithelial cells and inflammatory cells, could play an important role in the inflammatory process involved in neutrophil recruitment and exacerbations of COPD.…”

Section: Discussionmentioning

confidence: 99%

Muscarinic M3 receptor stimulation increases cigarette smoke-induced IL-8 secretion by human airway smooth muscle cells

Gosens¹,

Rieks²,

Meurs³

et al. 2009

Eur Respir J

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Acetylcholine is the primary parasympathetic neurotransmitter in the airways and is known to cause bronchoconstriction and mucus secretion. Recent findings suggest that acetylcholine also regulates aspects of remodelling and inflammation through its action on muscarinic receptors.In the present study, we aimed to determine the effects of muscarinic receptor stimulation on cytokine production by human airway smooth muscle cells (primary and immortalised cell lines). The muscarinic receptor agonists carbachol and methacholine both induced modest effects on basal interleukin (IL)-8 and -6 secretion, whereas the secretion of RANTES, eotaxin, vascular endothelial growth factor-A and monocyte chemoattractant protein-1 was not affected. Secretion of IL-8 and -6 was only observed in immortalised airway smooth muscle cells that express muscarinic M3 receptors. In these cells, methacholine also significantly augmented IL-8 secretion in combination with cigarette smoke extract in a synergistic manner, whereas synergistic effects on IL-6 secretion were not significant. Muscarinic M3 receptors were the primary subtype involved in augmenting cigarette smoke extract-induced IL-8 secretion, as only tiotropium bromide and muscarinic M3 receptor subtype selective antagonists abrogated the effects of methacholine.Collectively, these results indicate that muscarinic M3 receptor stimulation augments cigarette smoke extract-induced cytokine production by airway smooth muscle. This interaction could be of importance in patients with chronic obstructive pulmonary disease.

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Fluticasone, but not salmeterol, reduces cigarette smoke-induced production of interleukin-8 in human airway smooth muscle

Cited by 17 publications

References 38 publications

IκB kinase–driven nuclear factor-κB activation in patients with asthma and chronic obstructive pulmonary disease

IκB kinase–driven nuclear factor-κB activation in patients with asthma and chronic obstructive pulmonary disease

Role for TAK1 in cigarette smoke-induced proinflammatory signaling and IL-8 release by human airway smooth muscle cells

Muscarinic M3 receptor stimulation increases cigarette smoke-induced IL-8 secretion by human airway smooth muscle cells

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