Altered profile of circulating endothelial progenitor cells in obstructive sleep apnea

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S-maltoheptaose targets syndecan-bound effectors to reduce smoking-related neutrophilic inflammation.

Cigarette smoke induces injury and neutrophilic inflammation in the airways of smokers. The stability and activity of inflammatory effectors, IL8 and neutrophil elastase (NE), can be prolonged by binding to airway heparan sulfate (HS)/syndecan-1, posing risk for developing chronic obstructive pulmonary disease(COPD). We hypothesize that antagonizing HS/syndecan-1 binding of the inflammatory effectors could reduce smoking-related neutrophil-mediated airway inflammation. Analysis of bronchoalveolar lavage fluid(BALF) of COPD patients found both total and unopposed NE levels to be significantly higher among smokers with COPD than non-COPD subjects. Similar NE burden was observed in smoke-exposed rats compared to sham air controls. We chose sulfated-maltoheptaose(SM), a heparin-mimetic, to antagonize HS/sydecan-1 binding of the inflammatory mediators in airway fluids and lung tissues of the smoke-exposed rat model. Airway treatment with SM resulted in displacement of CINC-1 and NE from complexation with bronchio-epithelial HS/syndecan-1, dissipating the chemokine gradient for neutrophil flux across to the bronchial lumen. Following SM displacement of NE from shed HS/syndecan-1 in bronchial fluids, NE became accessible to inhibition by α1-antitrypsin endogenous in test samples. The antagonistic actions of SM against syndecan-1 binding of NE and CINC-1 in smoke-exposed airways suggest new therapeutic opportunities for modulating airway inflammation in smokers with SM delivery.published_or_final_versio

Serving Alone: The Social Service Sector in Hong Kong: Annual Report on the Civil Society in Hong Kong 2009

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Differential regulation of cytokine-and phorbol ester-induced activation of nuclear factor kappa B by Pseudomonas aeruginosa pyocyanin in human airway epithelial cells

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Serum superoxide dismutase levels correlate with disease activity markers in stable bronchiectasis

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The Natural and Built Environment Conservation Sector: Annual Report on the Civil Society in Hong Kong 2010

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Using Polyanionic Heparin Mimetics for the treatment of COPD

Poster Presentation - Theme 1: Cell biologyCOPD patients suffer from sustained inflammation leading to airway damage and deteriorating lung function caused by unopposed protease activity resulting from a1-antitrypsin resistant supramolecular complexes of neutrophil elastase and shed syndecan-1 in the airway. It was further shown that the action of the GAG digesting enzyme heparanase facilitates syndecan-1 shedding ...postprin

Elevated plasma adiponectin levels in patients with chronic obstructive pulmonary disease

BACKGROUND: Adiponectin is an anti-inflammatory adipokine that may play a role in chronic obstructive pulmonary disease (COPD) pathogenesis. OBJECTIVE: To investigate the relationship between adiponectin, interleukin (IL) 6, IL-8 and C-reactive protein (CRP) and COPD by evaluating these biomarkers in ever-smokers with or without the disease. METHOD: Plasma levels of adiponectin, IL-6, IL-8 and CRP were measured using commercially available kits in COPD patients (n = 71), healthy ever-smokers (n = 62) and non-smokers (n = 51). RESULTS: There were significant increases in plasma adiponectin, IL-6 and CRP in COPD patients (median [IQR] 4.39 μg/ml [2.68-6.98], 4.19 pg/ml [<2.40-6.40], 8.75 mg/l [4.26-40.63], respectively) compared to healthy ever-smokers (1.90 μg/ml [0.86-2.86], <2.40 pg/ml [<2.40-2.77], 3.71 mg/l [1.97-10.37 mg/l], respectively, P < 0.001) and non-smokers (1.76 μg/ml [1.34-2.52], <2.40 pg/ml [<2.40-2.78], 3.12 mg/l [2.11-5.71], respectively, P < 0.001). COPD patients had lower plasma IL-8 levels than healthy ever-smokers. Among ever-smokers with or without COPD, plasma adiponectin, IL-6 and CRP levels were inversely correlated with forced expiratory volume in 1 second (% predicted) after adjustment for age, body mass index, smoking status and pack-years. CONCLUSION: Our findings suggest that in COPD patients, adiponectin might be associated with COPD pathogenesis. © 2010 The Union.postprin

Chinese green tea ameliorates lung injury in cigarette smoke-exposed rats

Background: Epigallocatechin-3-gallate (EGCG), which has been shown to have potent antioxidant effect, comprises 80% of catechins in Chinese green tea. This study was to investigate whether cigarette smoke (CS) exposure would induce lung morphological changes and oxidative stress in the CS-exposed rat model, and whether Chinese green tea (Lung Chen tea with EGCG as its main active ingredient) consumption would alter oxidative stress in sera and lung leading to protection of CS-induced lung damage. Methods: Sprague-Dawley rats were randomly divided into four groups, i.e. sham air (SA), 4% CS, 2% Lung Chen tea plus SA or 4% CS. Exposure to SA or 4% CS was performed for 1 h/day for 56 days in ventilated smoking chambers. Sera and lung tissues were collected 24 h after last CS exposure for histology and all biochemical assays. Results: Airspace enlargement and goblet cell hyperplasia were observed after 56-day CS exposure alone, which were abolished in the presence of green tea consumption. Serum 8-isoprostane level was significantly elevated (p < 0.01) as well as lung superoxide dismutase (SOD) and catalase activities in CS-exposed rats compared to SA-exposed rats (p < 0.05), which returned to the levels of SA-exposed rats after Chinese green tea consumption. Conclusion: These results indicate that increased levels of systemic oxidative stress after CS exposure play an important role in the induction of lung damage. Chinese green tea may have the ability to suppress CS-induced oxidative stress that leads to protection of lung injury. © 2009 Elsevier Ltd. All rights reserved.postprin

Clinical value of ciliary assessment in bronchiectasis - a cross sectional study

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