Effect of fluticasone propionate on sputum of patients with chronic bronchitis and emphysema.

Llewellyn-Jones, Carol; Harris, Tim A. J.; Stockley, Robert A.

doi:10.1164/ajrccm.153.2.8564107

Cited by 115 publications

(68 citation statements)

References 25 publications

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“…The current data shows that inflammation in the larger airways is increased in the a 1 ATD subjects despite more using inhaled steroids (which would be expected to have a beneficial effect) [23] and the subjects being younger (which would also be associated with less inflammation in the larger airways) [31,32]. MPO concentrations were higher, as was the chemoattractant LTB 4 .…”

Section: Discussionmentioning

confidence: 61%

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Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Hill¹,

Bayley²,

Campbell³

et al. 2000

Eur Respir J

104

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Airways inflammation in chronic bronchitis is thought predominantly to be a direct consequence of neutrophil recruitment and release of elastase in response to factors such as cigarette smoke. The aims of this study were to assess the role of smoking and determine whether the serum elastase inhibitor α1‐antitrypsin (α1AT) influenced the process. Airways inflammation was compared between patients with chronic obstructive bronchitis with (n=39) and without (n=42) severe α1AT deficiency. The authors assessed the sputum concentration of the neutrophil chemoattractants interleukin‐8 (IL‐8) and leukotriene (LT)B4, myeloperoxidase (MPO) as a marker of neutrophil influx, neutrophil elastase activity and its natural inhibitors, α1AT and secretory leukoprotease inhibitor (SLPI). Finally serum α1AT was measured to determine the degree of protein leakage (sputum sol serum α1AT ratio). Compared to current smokers, the exsmokers had a lower concentration of the chemoattractant IL‐8 (p<0.05) and a lower MPO concentration, although this failed to reach conventional statistical significance (p=0.06). Patients with α1AT deficiency had greater inflammation in the larger airways with increased LTB4 (p<0.005), MPO (p<0.001), neutrophil elastase activity (p<0.01), protein leak (p<0.001), and were found to have a lower anti‐proteinase screen with both reduced sputum α1AT (p<0.001) and SLPI concentrations (p<0.05). The reduction in sputum interleukin‐8 levels in exsmokers may decrease neutrophil influx and thus explain the slower rate of neutrophil mediated progression of lung disease compared to subjects who continue to smoke. Patients with α1‐antitrypsin deficiency had greater inflammation suggesting that α1‐antitrypsin plays an important role in protecting the larger airways from the inflammatory effects of elastase activity and may explain their more rapid progression of disease.

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Section: Discussionmentioning

confidence: 61%

“…Sputum myeloperoxidase (MPO) and elastase activity was used to assess neutrophil influx and enzyme release, respectively, as described previously [23]. The lower limit of detection for elastase was 0.01 mM and samples below this level were classified as zero for statistical purposes.…”

Section: Assay Analysismentioning

confidence: 99%

Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Hill¹,

Bayley²,

Campbell³

et al. 2000

Eur Respir J

104

View full text Add to dashboard Cite

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“…22 ICS or oral steroids significantly reduce the chemotactic activity of neutrophils and increase the neutrophil elastase inhibitory capacity in induced sputum. 23,24 In addition, evidence from in vitro studies suggests that among the anti-inflammatory actions of steroids there is a reduction in the generation of ROS by neutrophils. 25 Acute smoke exposure increases the products of lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Levels in Exhaled Breath Condensate Associated With COPD and Smoking

Inonu¹,

Doruk²,

Sahin³

et al. 2012

Respir Care

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BACKGROUND: COPD is characterized by chronic air-flow limitation. Smoking is the most important factor in the pathogenesis of COPD. Smoking is associated with increased oxidative stress in the lungs. In this study our aim was to evaluate the differences in the burden of oxidative stress in patients with COPD, smokers, and non-smokers by measuring hydrogen peroxide (H 2 O 2 ), malondialdehyde (MDA), and 8-isoprostane levels in the exhaled breath condensate (EBC) samples. METHODS: Eighty subjects were included in the study. Group I (no. ‫؍‬ 25) had COPD, Group II (no. ‫؍‬ 26) was smokers, and Group III (no. ‫؍‬ 29) was nonsmokers. The severity of the COPD and dyspnea was assessed according to the results of pulmonary function tests (PFTs) and Medical Research Council (MRC) scale. RESULTS: The mean age of the subjects was 58 ؎ 8.9 years. While 8-isoprostane and H 2 O 2 levels were significantly higher in subjects with COPD (44.8 ؎ 40.2 pg/mL and 1.9 ؎ 0.8 mol/L) and smokers (41.3 ؎ 26 pg/mL and 1.7 ؎ 0.7 mol/L) than non-smokers (15.8 ؎ 6.9 pg/mL and 0.8 ؎ 0.4 mol/L), levels were similar between smokers and COPD subjects. MDA levels were similar between the 3 groups (P ‫؍‬ .31). There was no correlation between 8-isoprostane and H 2 O 2 levels and PFT parameters. There was a significant positive correlation between dyspnea grade on the MRC scale and 8-isoprostane levels (r ‫؍‬ 0.805, P < .001). CON-CLUSIONS: Even if respiratory function tests are within normal limits, oxidant burden in lungs of smokers is equivalent to that in COPD patients. 8-isoprostane could be useful in assessing symptom severity and health status of COPD patients.

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“…Sputum: MPO activity was used as a marker of sputum neutrophils [7], and measured by the colour released from the substrate o-dianisidine dihydrochloride (M6908; Sigma Chemical Company, Poole, UK) as described previously [13]. Samples from the same patient were analysed on the same plate and the same standard was used for all assays.…”

Section: Methodsmentioning

confidence: 99%

Bronchial inflammation in acute bacterial exacerbations of chronic bronchitis: the role of leukotriene B4

Crooks¹,

Bayley²,

Hill³

et al. 2000

Eur Respir J

201

148

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Neutrophils recruited to the airways in chronic obstructive pulmonary disease (COPD) are thought to mediate tissue destruction. Neutrophil recruitment is increased during bacterial exacerbations. The inflammatory process was studied in patients with an acute exacerbation of COPD in order to ascertain the role of leukotriene B 4 (LTB 4 ).The sputum of eight subjects with a bacterial exacerbation of COPD was analysed for neutrophil products (myeloperoxidase, elastase) and chemoattractants (interleukin-8 (IL-8) and LTB 4 ). The contribution of LTB 4 to the chemotactic activity of the sputum sol phase was determined using the LTB 4 receptor antagonist LY293111. The concentrations of the serum acute phase proteins a 1 -proteinase inhibitor, a 1 -antichymotrypsin and C-reactive protein were measured. All patients received appropriate broad-spectrum antibiotic treatment for 7±14 days.Initially, the sputum myeloperoxidase activity was high, indicating neutrophil influx; this was associated with high levels of IL-8 and LTB 4 . All these concentrations fell with treatment (p<0.01). The chemotactic activity of the sputum was raised on presentation and fell with treatment (p<0.01). LTB 4 contributed~30% of the total chemotactic activity on presentation; this diminished with therapy. All acute phase proteins were raised on presentation and fell with therapy (p<0.01).These findings suggest that leukotriene B 4 contributes to neutrophil influx into the airway in chronic obstructive pulmonary disease and may influence disease progresgression. Eur Respir J 2000; 15: 274±280.

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Effect of fluticasone propionate on sputum of patients with chronic bronchitis and emphysema.

Cited by 115 publications

References 25 publications

Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Airways inflammation in chronic bronchitis: the effects of smoking and alpha1-antitrypsin deficiency

Oxidative Stress Levels in Exhaled Breath Condensate Associated With COPD and Smoking

Bronchial inflammation in acute bacterial exacerbations of chronic bronchitis: the role of leukotriene B4

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