| Titre : |
Association of genetic variations in the CSF2 and CSF3 genes with lung function in smoking-induced COPD |
| Type de document : |
texte imprimé |
| Auteurs : |
J-Q. He, Auteur ; K. Shumansky, Auteur ; J.E. Connett, Auteur ; N.R. Anthonisen, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2008 |
| Collection : |
European Respiratory Journal num. 32 |
| Importance : |
p. 25-34 |
| Présentation : |
tab., graph. |
| Langues : |
Anglais (eng) |
| Catégories : |
[TABAC] étude
[TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
[TABAC] tabagisme:risque:facteur associé:génétique
|
| Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
| Résumé : |
Granulocyte-macrophage colony-stimulating factor (CSF), also known as CSF2, and granulocyte CSF, also known as CSF3, are important survival and proliferation factors for neutrophils and macrophages. The objective of the present study was to determine whether single nucleotide polymorphisms (SNPs) of CSF2 and CSF3 are associated with lung function in smoking-induced chronic obstructive pulmonary disease. In total, five SNPs of CSF2 and CSF3 were studied in 587 non-Hispanic white subjects with the fastest (n = 281) or the slowest (n = 306) decline of lung function selected from among continuous smokers in the National Heart, Lung, and Blood Institute Lung Health Study (LHS). These SNPs were also studied in 1,074 non-Hispanic white subjects with the lowest (n = 536) or the highest (n = 538) baseline lung function at the beginning of the LHS. An increase in the number of CSF3 -1719T alleles was significantly associated with protection against low lung function (odds ratio 0.73, 95% confidence interval 0.56-0.95), and was still significant after adjustment for multiple comparisons. There was also a significant association of a CSF3 haplotype with baseline levels of forced expiratory volume in one second. No association was found for CSF2 SNPs and lung function, nor was there evidence of epistasis. In conclusion, genetic variation in colony-stimulating factor 3 is associated with cross-sectionally measured lung function in smokers. |
| En ligne : |
https://erj.ersjournals.com/content/32/1/25.long |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8069 |
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| Titre : |
Cigarette smoke enhances {beta}-defensin 2 expression in rat airways via nuclear factor-{kappa}B activation |
| Type de document : |
texte imprimé |
| Auteurs : |
L. Chen, Auteur ; P.P. Sun, Auteur ; T. Wang, Auteur ; X. Wang, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2010 |
| Collection : |
European Respiratory Journal num. 36 |
| Importance : |
p.638-645 |
| Présentation : |
graph., ill. |
| Langues : |
Anglais (eng) |
| Catégories : |
[TABAC] chimie du tabac:fumée
[TABAC] étude
[TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
|
| Index. décimale : |
TA 3.2.2.1 Expérimentation |
| Résumé : |
β-defensin 2 (BD-2), an antimicrobial peptide, participates in airway defence. Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease. This study mainly aims to investigate the effect of CS on rat BD-2 (rBD-2) expression in rat airways. Rats were exposed to CS and treated with caffeic acid phenethyl ester (CAPE), a nuclear factor (NF)-κB inhibitor, or astragaloside IV (AS-IV), an active ingredient of Astragalus mongholicus. Besides the analysis of bronchoalveolar lavage fluid (BALF) and histological changes after CS exposure, rBD-2 expression was investigated with immunohistochemistry, reverse transcription PCR and ELISA. Total glutathione and nitric oxide (NO) levels in rat lungs were also detected. CS exposure markedly increased rBD-2 immunoreactivity, as well as rBD-2 mRNA and protein levels in rat airways, which were inhibited by CAPE treatment. Moreover, associated airway inflammation induced by CS was demonstrated by histological changes, increased cell counts and pro-inflammatory cytokines in BALF, and NF-κB activation and high levels of total glutathione and NO, which were all reversed by AS-IV in a dose-dependent fashion. In conclusion, CS exposure induces rBD-2 expression in rat airways via a NF-κB-dependent pathway, and AS-IV attenuates CS-induced airway inflammation due to its anti-inflammatory and antioxidant properties, at least partly through NF-κB inactivation. |
| En ligne : |
https://erj.ersjournals.com/content/36/3/638.long |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8075 |
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| Titre : |
Cigarette smoke extract reduces VEGF in primary human airway epithelial cells |
| Type de document : |
texte imprimé |
| Auteurs : |
J.V. Thaikoottathil, Auteur ; R.J. Martin, Auteur ; J. Zdunek, Auteur ; A. Weinberger, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2009 |
| Collection : |
European Respiratory Journal num. 33:4 |
| Importance : |
p.835-843 |
| Présentation : |
tab., tab., ill. |
| Langues : |
Anglais (eng) |
| Catégories : |
[TABAC] étude
[TABAC] tabagisme:effet du tabac:effet sur l'immunité
|
| Index. décimale : |
TA 3.2.2.2.1 Interactions avec d'autres facteurs pathogènes |
| Résumé : |
Reduced vascular endothelial growth factor (VEGF) has been reported in bronchoalveolar lavage fluid and lungs of severe emphysema patients. Airway epithelial cells (AEC) are exposed to various environmental insults like cigarette smoke and bacterial infections, but their direct effect on VEGF production in well-differentiated primary human AEC remains unclear. The current authors determined the effect of cigarette smoke extract (CSE) alone and in combination with Mycoplasma pneumoniae (Mp) on VEGF production in well-differentiated primary normal human bronchial epithelial (NHBE) and small airway epithelial cells (SAEC) in air-liquid interface cultures. Secretion and expression of VEGF were determined by ELISA and real-time RT-PCR, respectively. Cell growth, apoptosis, extracellular signal-regulated kinase (ERK)1/2 and protein kinase (PK)C signalling pathways were evaluated to further dissect VEGF regulation under CSE treatment. CSE significantly reduced VEGF secretion in NHBE and SAEC. In SAEC, Mp alone significantly increased the VEGF, while the presence of CSE attenuated Mp-induced VEGF production. While ERK inhibitor reduced VEGF secretion only in NHBE, a PKC inhibitor significantly decreased VEGF secretion in both NHBE and SAEC. In conclusion, direct cigarette smoke extract exposure significantly reduced vascular endothelial growth factor production in well-differentiated primary human airway epithelial cells, in part through modifying extracellular signal-regulated kinase 1/2 and protein kinase C signalling pathways. |
| En ligne : |
https://erj.ersjournals.com/content/33/4/835.long |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8063 |
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| Titre : |
Cigarette smoke induces CXCL8 production by human neutrophils via activation of TLR9 receptor |
| Type de document : |
texte imprimé |
| Auteurs : |
E. Mortaz, Auteur ; I.M. Adcock, Auteur ; K. Ito, Auteur ; A.D. Kraneveld, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2010 |
| Collection : |
European Respiratory Journal num. 36 |
| Importance : |
p. 1143-1154 |
| Présentation : |
graph. |
| Langues : |
Anglais (eng) |
| Catégories : |
[TABAC] chimie du tabac:fumée
[TABAC] étude
[TABAC] tabagisme:effet du tabac:effet sur l'immunité
[TABAC] tabagisme:pathologie:pathologie respiratoire:broncho-pneumopathie chronique obstructive
|
| Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
| Résumé : |
Chronic obstructive pulmonary disease (COPD) is a major health problem and cigarette smoke is the main risk factor for the development of COPD. The characteristic changes in airway morphology, inflammatory cell infiltration and mediator expression in COPD may result from direct effects of cigarette smoke on airway cells. Toll-like receptors (TLRs) are key elements in pathogen recognition by the host immune system. Although TLRs have been intensely studied in innate immunity and infection, their critical role in noninfectious challenges has only recently emerged. Here we investigate whether cigarette smoke induces TLR9 signalling in human neutrophils. Human neutrophils were isolated from buffy coat and exposed to cigarette smoke extract. The production of CXC chemokine ligand (CXCL)8 was measured as a functional readout and the role of TLR9 signalling was investigated. Cigarette smoke extract induced CXCL8 release via TLR9 activation in neutrophils, which was confirmed in TLR9 stably transfected human embryonic kidney 293 cells. Moreover, cigarette smoke extract upregulated the expression of TLR9 and the upregulated expression was suppressed by N-acetylcysteine. TLR9 mediates cigarette smoke-induced release of CXCL8 and this may contribute to the accumulation of neutrophils and inflammation within the airways of smokers. |
| En ligne : |
https://erj.ersjournals.com/content/36/5/1143 |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8071 |
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Exemplaires (1)
|
| TA 005622 | TA 3.2.2.4 MOR C | Article/Périodique | Bibliothèque FARES | Tabac | Consultation sur place
Exclu du prêt |
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| Titre : |
Diagnosis and treatment of nicotine dependence with emphasis on nicotine replacement therapy : a status report |
| Type de document : |
document électronique |
| Auteurs : |
David J.K. Balfour, Auteur ; Neal L. Benowitz, Auteur ; Karl Fagerström, Auteur ; M. Kunze, Auteur ; U. Keil, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2000 |
| Collection : |
European Respiratory Journal num. 21 |
| Importance : |
p.438-445 |
| Langues : |
Anglais (eng) |
| Catégories : |
[TABAC] sevrage tabagique:méthode de sevrage:méthode individuelle:approche pharmacologique:substitution nicotinique
[TABAC] tabagisme:dépendance tabagique:dépendance pharmacologique
[TABAC] tabagisme:évaluation du tabagisme:test de dépendance à la nicotine
|
| Index. décimale : |
TA 4.2.2.1 Dépendance à la nicotine |
| Résumé : |
Tobacco use is a global health care problem. Repetitive exposure to nicotine produces neuroadaptation resulting in nicotine dependence. Cigarette smoking is particularly addictive due to the repeated delivery of bolus doses of nicotine to the bloodstream. Although compulsive tobacco use is sustained by nicotine addiction, it is the toxic combustion products in tobacco smoke such as carbon monoxide and oxidant gases that adversely affect the cardiovascular system. Smoking cessation produces significant health benefits and is a very cost-effective intervention. Evidence that nicotine is the addictive component of tobacco provides the rationale for using nicotine replacement therapy to aid cessation. Nicotine replacement therapy doubles successful smoking cessation rates and evidence-based guidelines for the treatment of tobacco addiction recommend routine use of nicotine replacement therapy, particularly in heavily dependent smokers. Success rates of up to 40% can be achieved in specialist clinics. Despite early concerns regarding the safety of nicotine replacement therapy in smokers with heart disease, it is now clear that the health risks of using nicotine replacement therapy to assist such patients to stop, or significantly reduce, smoking far outweigh any treatment-related risks. |
| En ligne : |
https://doi.org/10.1053/euhj.1999.1949 |
| Format de la ressource électronique : |
Article en ligne |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=10348 |
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| Titre : |
Effect of low-dose thephylline plus beclometasone on lung function in smokers with asthma : a pilot stydy |
| Type de document : |
texte imprimé |
| Auteurs : |
M. Spears, Auteur ; I. Donnelly, Auteur ; M. Brannigan, Auteur ; K. Ito, Auteur |
| Editeur : |
European Respiratory Society (ERS) |
| Année de publication : |
2009 |
| Collection : |
European Respiratory Journal num. 33 suppl. |
| Importance : |
p. 1010-1017 |
| Présentation : |
tab., graph. |
| Langues : |
Anglais (eng) |
| Catégories : |
[PROMOSAN] asthme:traitement de l'asthme
[TABAC] étude
[TABAC] tabagisme:pathologie:pathologie respiratoire:asthme
|
| Index. décimale : |
TA 3.2.2.4 Pathologies respiratoires (sauf 3.2.2.1, 3.2.2.2, 3.2.2.3) |
| Résumé : |
Smoking is common in asthma and is associated with worse asthma control and a reduced therapeutic response to corticosteroids. The present authors hypothesised that treating smokers with asthma with low-dose theophylline added to inhaled corticosteroids would enhance steroid sensitivity and thereby improve lung function and symptoms. In a double-blind, parallel group exploratory trial, 68 asthmatic smokers were randomised to one of three treatments for 4 weeks: inhaled beclometasone (200 microg day(-1)), theophylline (400 mg day(-1)) or both treatments combined. Outcome measures included change in lung function and Asthma Control Questionnaire (ACQ) scores. At 4 weeks, theophylline added to inhaled beclometasone produced an improvement in peak expiratory flow (39.9 L min(-1), 95% confidence intervals (CI) 10.9-68.8) and ACQ score (-0.47, 95% CI -0.91- -0.04) and a borderline improvement in pre-bronchodilator forced expiratory volume in one second (mean difference 165 mL, 95% CI -13-342) relative to inhaled corticosteroid alone. Theophylline alone improved the ACQ score (-0.55, 95% CI -0.99- -0.11), but not lung function. In the present pilot study, the combination of low-dose theophylline and inhaled beclometasone produced improvements in both lung function and symptoms in a group of smokers with asthma. Larger trials are required to extend and confirm these findings. |
| En ligne : |
https://erj.ersjournals.com/content/33/5/1010 |
| Permalink : |
https://biblio.fares.be/opac_css/index.php?lvl=notice_display&id=8065 |
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Ajouter le résultat dans votre panier Affiner la rechercheAssociation of genetic variations in the CSF2 and CSF3 genes with lung function in smoking-induced COPD / J-Q. He (2008)
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