Abstract
Background: Sestrin 2, Endocan, and Sirtuin 1 are distinct molecules with some biologic actions associated with asthma pathophysiology. The aim of the present study was to determine the molecular level differences attributable to underlying asthma severity. Methods: We initially recruited 85 asthmatics with a wide spectrum of severity. All of the patients were optimally treated according to current guidelines. Demographics, test results of lung function, and treatment regimes of all patients were recorded. Sestrin 2, Endocan, and Sirtuin 1 were measured in different biological samples (sputum with two processing methods and serum). Results: A total of 60 patients (35 with severe asthma) were analyzed, since 25 patients failed to produce an adequate sample of sputum. Patients with severe asthma showed significantly higher values for Sestrin 2 [pg/mL], measured in both sputum supernatant and cell pellet, compared to those with mild to moderate asthma [9524 (5696, 12,373) vs. 7476 (4265, 9273) p = 0.029, and 23,748 (15,280, 32,742) vs. 10,084 (3349, 21,784), p = 0.008, respectively]. No other significant differences were observed. No significant associations were observed between biomarkers, inflammatory cells, and lung function. Conclusion: Sestrin 2 is increased in patients with severe asthma as part of a mechanism that may modify structural alterations through the imbalance between oxidative stress and antioxidant activity.
Highlights
Inflammation and structural and functional abnormalities within the airways are key features of asthma [1]
The poor response to steroids might be partly attributed to tissue repair, remodeling, and airway inflammation, which are amplified in Severe refractory asthma (SRA) [4]
We demonstrated that Sestrin 2 levels were higher in both sputum supernatant and cell pellet of patients with severe asthma compared to those with milder forms of the disease, whereas neither Endocan nor Sirtuin 1 (SIRT1) serum levels differed between patients with different asthma severity
Summary
Inflammation and structural and functional abnormalities within the airways are key features of asthma [1]. Distinct molecular mechanisms and biomarkers in different biological samples have been identified and linked to clinical asthma phenotypes [2]. These processes are well-documented, their expressions vary across the heterogeneous spectrum of asthma severity. Sestrin 2, Endocan, and Sirtuin 1 were measured in different biological samples (sputum with two processing methods and serum). Patients with severe asthma showed significantly higher values for Sestrin 2 [pg/mL], measured in both sputum supernatant and cell pellet, compared to those with mild to moderate asthma [9524 (5696, 12,373) vs 7476 (4265, 9273) p = 0.029, and 23,748 (15,280, 32,742) vs 10,084 (3349, 21,784), p = 0.008, respectively]. No significant associations were observed between biomarkers, inflammatory cells, and lung function. Conclusion: Sestrin 2 is increased in patients with severe asthma as part of a mechanism that may modify structural alterations through the imbalance between oxidative stress and antioxidant activity
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