Asthma and cigarette smoking

Thomson, Neil C.; Chaudhuri, Rekha; Livingston, Eric W.

doi:10.1183/09031936.04.00039004

Cited by 472 publications

(313 citation statements)

References 155 publications

(193 reference statements)

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“…To the best of the current authors' knowledge, this is the first study to report on this matter, as most previous studies addressing atopy versus smoking have focused on the tobacco-induced increased risk of developing atopy and asthma [21,22] and on the increased severity, inflammation and progress of atopic diseases, such as asthma in smokers [23][24][25].…”

Section: Discussionmentioning

confidence: 97%

Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

Glader

Eldh²,

Bozinovski³

et al. 2008

Eur Respir J

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Clinical studies have indicated increased gelatinase activity in the airways of patients suffering from chronic obstructive pulmonary disease caused by tobacco smoke. The present study aimed to determine whether acute exposure to tobacco smoke per se causes a substantial and lasting impact on gelatinases and their inhibitors in the peripheral airways of atopic and nonatopic human subjects.Bronchoscopy with bronchoalveolar lavage (BAL) was performed on occasional smokers with and without atopy before and after smoking 10 cigarettes over a 48-h period. Samples from a group of never-smokers not exposed to tobacco smoke served as controls. Gelatinase identity and activity were measured using zymography, and gelatinase activity assay and concentrations of matrix metalloproteinase (MMP)-2, MMP-9, tissue inhibitor of MMP (TIMP)-1 and TIMP-2 were measured using ELISA.The results revealed no pronounced changes in identity, net activity or concentration of the gelatinases or changes in concentrations of TIMP-1 and TIMP-2 in BAL fluid before and after acute exposure to tobacco smoke.In conclusion, the present experimental study indicates that acute exposure to tobacco smoke does not cause any substantial impact on gelatinases or their inhibitors in the peripheral airways, irrespective of atopy status, a finding that is compatible with the fact that it takes many years of tobacco smoking to establish chronic obstructive pulmonary disease. KEYWORDS: Chronic obstructive pulmonary disease, macrophage, matrix metalloproteinase 9, neutrophils, tissue inhibitor of matrix metalloproteinase

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Section: Discussionmentioning

confidence: 97%

Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

Glader

Eldh²,

Bozinovski³

et al. 2008

Eur Respir J

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“…Little is known regarding the influence of smoking on the bronchial inflammatory response in asthma. Only few data are available on airway pathology in smoking asthmatics, as reviewed by THOMSON et al [6]. The main findings are reduced eosinophils in both induced sputum and peripheral blood, while neutrophils are increased in induced sputum samples.…”

mentioning

confidence: 99%

Reduced bronchial CD4+ T-cell density in smokers with occupational asthma

Sjåheim¹,

Kongerud²,

Bjørtuft³

et al. 2006

Eur Respir J

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Cigarette smoking may alter bronchial inflammation in asthma. Multicolour immunohistofluorescent examination on bronchial cryosections was used to examine bronchial inflammatory cell infiltrate in patients with occupational asthma. Monoclonal antibodies to CD3, CD4, CD8, T-cell receptor-d1, CD68 and human leukocyte antigen-DR were combined to identify Tcell subsets and macrophages in bronchial biopsies from 20 workers with occupational asthma (12 smokers and eight nonsmokers), 15 healthy workers (seven smokers and eight nonsmokers) and 10 nonsmoking, nonexposed controls.The increased subepithelial CD4+ T-cell density in nonsmoking asthmatics was not present in smoking asthmatics, who had the lowest CD4+ T-cell density of all groups. The decreased subepithelial CD4+ and CD8+ T-cell density correlated with a reduction in lung function, as measured by percentage predicted forced expiratory volume in one second, in smoking asthmatics only. Although smoking asthmatics had a significantly increased number of intraepithelial CD8+ T-cells and macrophages compared with nonsmoking asthmatics, the proportion of cd-T-cells was significantly decreased in both asthmatic groups.Smoking asthmatics had a distinctly different distribution of T-cell subsets compared with nonsmoking asthmatics. The accumulation of subepithelial CD4+ T-cells, which was observed in nonsmoking asthmatics, appeared to be inhibited in smoking asthmatics, suggesting a smokinginduced bronchial immune modulation, at least in occupational asthma in the aluminium industry.

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“…(3) Prevalence of active and passive smoking in a population of patients with asthma* function characteristics, as well as data related to asthma profile and smoking status, are presented in Table 1.…”

mentioning

confidence: 99%

“…Although there is still little information specifically regarding asthma patients who smoke, one group of authors reported that the prevalence of active smokers among asthma patients can range from 17% to 35%. (3) Early detection of active or passive smoking in asthma patients is essential so that smoking cessation programs can be offered to them. Such programs, in addition to decreasing the potential risk for uncontrolled asthma, will principally prevent individuals from developing asthma and COPD in the future.…”

mentioning

confidence: 99%

Prevalência de tabagismo ativo e passivo em uma população de asmáticos

et al. 2009

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Smoking causes an intense inflammatory reaction in the airways and is associated with worse clinical outcomes in patients with asthma. The objective of this study was to determine the prevalence of active and passive smoking in a population of patients with asthma. The sample of asthma patients (n = 100) consisted of 47 nonsmokers, 33 former smokers, 17 passive smokers and 3 active smokers. Most had moderate or severe asthma. Mean exhaled CO was 9.34 ppb in smokers, 4.19 ppb in passive smokers, 3.98 ppb in nonsmokers and 3.98 ppb in former smokers. We conclude that the prevalence of exposure to tobacco smoke is high among asthma patients.Keywords: Smoking; Asthma; Prevalence. ResumoO tabagismo causa intensa reação inflamatória nas vias aéreas e, em asmáticos, está associado com piores desfechos clínicos. O objetivo desse estudo foi determinar a prevalência de tabagismo ativo e passivo em uma população de asmáticos. A amostra de pacientes com asma (n = 100) consistiu em 47 não-fumantes, 33 ex-fumantes e 3 fumantes ativos. A maioria dos pacientes tinha asma moderada ou grave. A média de CO exalado foi de 9,34 ppb nos tabagistas atuais, 4,19 ppb nos fumantes passivos e 3,98 ppb tanto nos não-fumantes quanto nos ex-fumantes. Concluímos que a prevalência da exposição à fumaça do tabaco é alta entre asmáticos.

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Asthma and cigarette smoking

Cited by 472 publications

References 155 publications

Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

Impact of acute exposure to tobacco smoke on gelatinases in the bronchoalveolar space

Reduced bronchial CD4+ T-cell density in smokers with occupational asthma

Prevalência de tabagismo ativo e passivo em uma população de asmáticos

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