R. Germinario, E. Andriani, P. Tondo, P. Soccio, A. la Grasta, I. Cafagna, D. Lacedonia, F. Dell’Olio & G. Scioscia.
Abstract
Exhaled breath analysis offers a painless window into airway inflammation, yet its clinical adoption is limited by a shortage of robust biomarkers. Hydrogen sulfide () has been detected in biological fluids, but its diagnostic value across asthma severities is not well established. In this study, we integrated an electrochemical sensor with a detection limit of 1 ppb into the MISTRAL platform. We evaluated exhaled in a prospective cohort of 28 adult asthmatic patients. Mean exhaled concentrations were significantly higher in individuals with mild-to-moderate asthma () than in those with severe asthma (; one‑tailed t‑test , ). In early-stage disease, levels negatively correlated with maximal expiratory flow MEF, with a similar trend for MEF, whereas in severe asthma, positive but not fully statistically significant correlations emerged with FEV/FVC ratio, and vital capacity VC. These findings reveal a biphasic pattern: elevated may signify a compensatory antioxidant response that collapses as damage in the medium-to-peripheral airways progresses. The plug-and-play MISTRAL platform thus enables real-time, point-of-care assessment of exhaled as a promising, and complementary biomarker to FeNO and blood eosinophil count, offering a rapid, non-invasive indicator of disease control, treatment responsiveness, and exacerbation risk.
Conclusions
The MISTRAL platform was upgraded by integrating an electrochemical HS sensor to investigate the role of hydrogen sulfide in modulating asthma-induced airway inflammation. Exhaled HS levels were measured in a total of 12 patients with mild-to-moderate asthma and 16 patients with severe asthma. Lower exhaled HS levels were observed in patients with severe asthma compared to those with mild-to-moderate asthma, suggesting its anti-inflammatory and protective role against lung tissue injury and exacerbation risk. Reduced exhaled HS in advanced stages may reflect the failure of an endogenous compensatory mechanism mediated by this molecule, resulting in increased airway obstruction, decreased lung volume, and heightened need for intensive pharmacological therapies. In contrast, in the earlier stages, this mechanism may still be partially active, but not sufficient to protect the medium-to-peripheral airways. The findings may indicate a potentially biphasic pattern of HS in asthma pathogenesis, with exhaled levels varying according to the stage of disease progression. Taking this into account, the detection of exhaled HS via a portable, low-cost, plug-and-play sensor may provide enhanced predictive insight into treatment response to biologics, potentially enriching the current panel of asthma biomarkers. This approach may open new perspectives in personalized medicine by enabling a multidimensional characterization of asthma and potentially facilitating more rapid outpatient follow-up.
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