Endogenous Hydrogen Sulfide in Patients With COPD

Chen, Yahong; Yao, Wan-zhen; Geng, Bin; Ding, Yanling; Lu, Ming; Zhao, Mingjing; Tang, Chaoshu

doi:10.1378/chest.128.5.3205

Cited by 234 publications

(196 citation statements)

References 27 publications

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“…We previously found that exhaled H 2 S levels positively correlate with exhaled NO in patients with COPD. 9,13,25 This close relationship between exhaled NO and H 2 S highlights the possibility that H 2 S may be useful as a COPD biomarker. Similar to previous studies, we observed no correlation between exhaled H 2 S and predicted FEV 1 .…”

Section: Discussionmentioning

confidence: 95%

“…In contrast, patients with exacerbations of COPD have significantly decreased levels of serum H 2 S. Thus, levels of endogenous H 2 S may represent a potential indicator of COPD severity. [9][10][11] However, the relationship between levels of exhaled H 2 S and airway or systemic inflammation has not yet been determined. Recently, the analysis of signaling molecules present in exhaled air has become a popular technique for noninvasive assessment of airway inflammation.…”

Section: Introductionmentioning

confidence: 99%

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Exhaled Hydrogen Sulfide Predicts Airway Inflammation Phenotype in COPD

et al. 2014

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BACKGROUND: The role of exhaled H 2 S as a marker of airway inflammation and its relationship with COPD severity remain to be determined. METHODS: Airway inflammation was classified in 77 COPD subjects based on the presence of inflammatory cells in induced sputum. We investigated the association between disease phenotype and exhaled H 2 S, lung function, and plasma levels of several inflammatory factors, including tumor necrosis factor alpha, interleukin-8, and leukotriene B 4 . RESULTS: In total, 33.77% of enrolled COPD subjects were diagnosed with eosinophilia. These subjects had a longer disease course, smoked fewer cigarettes, and experienced more frequent exacerbation events before study enrollment. However, they also had worse lung function and larger residual volume, they demonstrated greater changes in FEV 1 following bronchodilator inhalation. Although levels of plasma inflammatory factors did not significantly differ between subjects with and without eosinophilia, subjects without eosinophilia had significantly higher levels of exhaled H 2 S (9.19 ؎ 2.74 vs 7.24 ؎ 1.68 parts per billion, P ‫؍‬ .01). Furthermore, exhaled H 2 S levels were negatively correlated with induced sputum eosinophils (r ‫؍‬ ؊0.45, P ‫؍‬ .05), and positively correlated with inspiratory capacity in COPD subjects (r ‫؍‬ 0.51, P ‫؍‬ .026), but did not correlate significantly with plasma inflammatory factors. A cut-off value of 7.10 parts per billion of exhaled H 2 S predicted a non-eosinophilic phenotype with 68.6% sensitivity and 77.9% specificity. CONCLUSIONS: Exhaled levels of H 2 S were lower in subjects with eosinophilia. Increased levels of exhaled H 2 S predicted a non-eosinophilic phenotype in our study population. Key words: chronic obstructive pulmonary disease; airway inflammation phenotype; eosinophilia; hydrogen sulfide. [Respir Care 2015;60(2):251-258.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Exhaled Hydrogen Sulfide Predicts Airway Inflammation Phenotype in COPD

et al. 2014

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“…Levels of H 2 S decreased with progressively worsening respiratory failure. In these studies, serum H 2 S levels negatively correlated with sputum neutrophil counts but positively correlated with sputum lymphocyte [60] and macrophage [62] counts, lung function (forced expiratory volume in 1 s) [61,62] and serum • NO, suggesting that during COPD, H 2 S synthesis is induced in the lung to promote bronchial smooth muscle dilatation to improve airflow and limit inflammatory signaling.…”

Section: H 2 S and Inflammatory Lung Diseasementioning

confidence: 85%

“…Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation throughout the airways, parenchymal and pulmonary vasculature, resulting in substantial airflow obstruction. Using a sulfide-specific electrode, Chen et al showed significantly higher serum H 2 S levels in patients with COPD compared with age-matched control subjects or patients with acute exacerbation of COPD [61,62]. Levels of H 2 S decreased with progressively worsening respiratory failure.…”

Section: H 2 S and Inflammatory Lung Diseasementioning

confidence: 99%

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

Whiteman

Winyard

2011

Expert Review of Clinical Pharmacology

279

232

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“…In tissue culture media, the concentrations of sulfane-sulfur is situated at any time below the nanomolar range [71]. The normal H 2 S concentration measured in mammalian plasmas usually ranges from 10 to 100 μM with a mean average turning around 40-50 μM [19,21,82,83]. This H 2 S plasma level, appearing as the net product of organs possessing C S and C L enzymes and supplemented by the non-enzymatic conversion of S, flows transiently into the vasculature and freely penetrates into all body cells.…”

Section: Roles Played By Hydrogen Sulfidementioning

confidence: 99%

The Oxidative Stress of Hyperhomocysteinemia Results from Reduced Bioavailability of Sulfur-Containing Reductants

Ingenbleek¹

2011

TOCCHEMJ

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Vegetarian subjects consuming subnormal amounts of methionine (Met) are characterized by subclinical protein malnutrition causing reduction in size of their lean body mass (LBM) best identified by the serial measurement of plasma transthyretin (TTR). As a result, the transsulfuration pathway is depressed at cystathionine--synthase (C S) level triggering the upstream sequestration of homocysteine (Hcy) in biological fluids and promoting its conversion to Met. Maintenance of beneficial Met homeostasis is counterpoised by the drop of cysteine (Cys) and glutathione (GSH) values downstream to C S causing in turn declining generation of hydrogen sulfide (H 2 S) from enzymatic sources. The biogenesis of H 2 S via non-enzymatic reduction is further inhibited in areas where earth's crust is depleted in elemental sulfur (S 8 ) and sulfate oxyanions. Combination of subclinical malnutrition and S 8 -deficiency thus maximizes the defective production of Cys, GSH and H 2 S reductants, explaining persistence of unabated oxidative burden. The clinical entity increases the risk of developing cardiovascular diseases (CVD) and stroke in underprivileged plant-eating populations regardless of Framingham criteria and vitamin-B status. Although unrecognized up to now, the nutritional disorder is one of the commonest worldwide, reaching top prevalence in populated regions of Southeastern Asia. Increased risk of hyperhomocysteinemia and oxidative stress may also affect individuals suffering from intestinal malabsorption or westernized communities having adopted vegan dietary lifestyles.

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Endogenous Hydrogen Sulfide in Patients With COPD

Cited by 234 publications

References 27 publications

Exhaled Hydrogen Sulfide Predicts Airway Inflammation Phenotype in COPD

Exhaled Hydrogen Sulfide Predicts Airway Inflammation Phenotype in COPD

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

The Oxidative Stress of Hyperhomocysteinemia Results from Reduced Bioavailability of Sulfur-Containing Reductants

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