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Hydrogen sulfide (H2S) has recently been recognised as the third important gas-signalling molecule, besides nitric oxide and carbon monoxide. H2S has been reported to be produced by many cell types in mammalian tissues and organs throughout the actions of H2S-generating enzymes or redox reactions between the oxidation of glucose and element of sulfur. Although the pathological role of H2S has not yet been fully elucidated, accumulative data suggest that H2S may have biphasic effects. Briefly, it mainly has anti-inflammatory and antioxidant roles, although it can also have pro-inflammatory effects under certain conditions where rapid release of H2S in tissues occur, such as sepsis. To date, there have been several clinical studies published on H2S in respiratory disorders, including asthma and chronic obstructive pulmonary disease (COPD). According to previous studies, H2S is detectable in serum, sputum, and exhaled breath, although a gold standard method for detection has not yet been established. In asthma and COPD, H2S levels in serum and sputum can vary depending on the underlying conditions such as an acute exacerbation. Furthermore, sputum H2S in particular correlates with sputum neutrophils and the degree of airflow limitation, indicating that H2S has potential as a novel promising biomarker for neutrophilic airway inflammation for predicting current control state as well as future risks of asthma. In the future, concurrent measures of H2S with conventional inflammatory biomarkers (fractional exhaled nitric oxide, eosinophils etc) may provide more useful information regarding the identification of inflammatory phenotypes of asthma and COPD for personalised treatment.

Background: There is evidence that neutrophils are increased in the airway of severe disease or acute exacerbations of asthma. The mechanisms by which neutrophils are recruited to the airways and contribute to the pathophysiology of asthma remain to be elucidated. Tumor necrosis factor (TNF-α), which can induce both tissue accumulation and activation of neutrophils and eosinophils, has been shown to be increased in the airways of severe asthma. The objective of this study is to evaluate whether TNF-α is associated with neutrophilic inflammation in asthma. Methods: Following an inhalation of hypertonic saline, induced sputum was obtained from 9 healthy controls, 9 mild persistent asthma patients who were treated with low-dose inhaled corticosteroids; and 7 severe persistent asthma patients who were treated with combinations of drugs including high-dose inhaled corticosteroids, oral prednisolone, bronchodilators, and leukotriene receptor antagonist. After 0.1% dithiothreitol (DTT) homog- enization, they were examined for total cell count, cellular differentiation, and the concentrations of TNF-α and myeloperoxidase (MPO). Results: The concentration of TNF-α was not correlated with neutrophils in healthy controls or mild asthma patients. In sputum from severe asthma patients, however, the concentration of TNF-α is significantly correlated with both the percentage of neutrophils and the concentration of MPO. The concentration of TNF-α is not correlated with the percentage of eosinophils in healthy controls, mild asthma patients, or severe asthma patients. Conclusions: TNF-α may be a contributing molecule for both accumulation and activation of neutrophils in the airways of severe asthma.