Cigarette smoke induces CXCL8 production by human neutrophils via activation of TLR9 receptor

Mortaz, Esmaeil; Adcock, Ian M.; Ito, Kiminari; Kraneveld, Aletta D.; Nijkamp, Frans P.; Folkerts, Gert

doi:10.1183/09031936.00062209

Cited by 77 publications

(58 citation statements)

References 57 publications

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“…Interestingly, it has been suggested that TLRs may mediate CS-induced signaling as CSE-induced IL-8 release was shown to be dependent on TLR4 and TLR9 activation in macrophages and neutrophils, respectively (20,24). In addition, CS-induced neutrophilia and inflammatory cytokine production are attenuated in mice lacking TLR4 or the downstream MyD88 adapter (8,22).…”

Section: Discussionmentioning

confidence: 96%

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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Section: Discussionmentioning

confidence: 96%

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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“…CXCL-8 has significant neutrophil chemoattractant and activating properties. Increasing production of CXCL-8 may contribute to the accumulation of neutrophils and inflammation in COPD (Mortaz et al 2010).…”

Section: Introductionmentioning

confidence: 99%

Low-dose theophylline restores corticosteroid responsiveness in rats with smoke-induced airway inflammation

Sun

Gong

et al. 2012

Can. J. Physiol. Pharmacol.

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Patients with chronic obstructive pulmonary disease (COPD) respond poorly to corticosteroids. Histone deacetylase-2 (HDAC-2) plays a pivotal role in many cases of steroid insensitivity. The main aim of this study was to restore the smoking-induced reduction in corticosteroid sensitivity by increasing HDAC-2 activity using low-dose theophylline. Rats were exposed to cigarette smoke (CS) and treated with budesonide and two doses of theophylline. Besides the pathologic examination and cell counting in the bronchoalveolar lavage fluid (BALF), the expression of HDAC-2 and CXC chemokine ligand-8 (CXCL-8) were measured. Airway inflammation induced by CS was demonstrated by pathologic changes of lung tissue and increased level of CXCL-8. CS exposure also markedly decreased HDAC-2 expression. Moreover, a negative correlation was found between HDAC-2 activity and a lung destruction index. The index was restored to control levels with inhaled corticosteroid treatment in combination with a low, not a high, dose of theophylline. These results indicate that low-dose theophylline might provide protection from smoke damage and improve the anti-inflammatory effects of steroids by increasing HDAC-2 activity.

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“…More recently, Mortaz et al (2010) elaborated on the role of human TLR9 in cigarette smoke-induced signaling. They demonstrated in vitro that TLR9 is involved in cigarette smoke-induced CXCL8 production by plasmacytoid DCs and neutrophils.…”

Section: B Cigarette Smoke-induced Toll-like Receptor Activationmentioning

confidence: 99%

Dual Role of Toll-Like Receptors in Asthma and Chronic Obstructive Pulmonary Disease

et al. 2012

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Cigarette smoke induces CXCL8 production by human neutrophils via activation of TLR9 receptor

Cited by 77 publications

References 57 publications

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

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

Low-dose theophylline restores corticosteroid responsiveness in rats with smoke-induced airway inflammation

Dual Role of Toll-Like Receptors in Asthma and Chronic Obstructive Pulmonary Disease

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