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Updated: Jun 30, 2026

Methodology for Sputum Induction and Laboratory Processing
Published on: December 17, 2017
Increased induced sputum ITGB5 expression was correlated with airway inflammation and lung function in asthma
Yuxia Liang1,2, Lingzi Lei1, Lu Qin1
1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Background:
ITGB5 encodes integrin subunit beta 5 of that has been implicated in the eosinophilic asthma phenotype. However, the secretory profile of ITGB5 in induced sputum and its clinical significance in asthma remains poorly understood.
Objective:
This study aimed to measure ITGB5 levels in induced sputum supernatant from asthma patients and investigate its potential clinical implications.
Methods:
We enrolled 78 participants (18 healthy controls and 60 asthma patients) and quantified ITGB5 protein levels in induced sputum supernatant using ELISA. Correlations between ITGB5 and inflammatory markers, as well as airway obstruction parameters, were analyzed. Subsequently, we performed comparative analyses to evaluate variations in inflammatory cytokines between high- and low-ITGB5 expression subgroups.
Results:
Induced sputum ITGB5 levels were significantly elevated in asthma patients and markedly increased following inhaled corticosteroid (ICS) treatment. ITGB5 levels showed positive correlations with Th2-associated cytokines (IL-4, IL-5, IL-13, IL-25, IL-33, and TSLP) and Th2 signature genes (SERPINB2, CLCA1, and POSTN). Notably, IL-5, FeNO, and POSTN were significantly higher in the high-ITGB5(n = 30) than the low- ITGB5 (n = 30) expression group. Furthermore, sputum ITGB5 levels were inversely associated with pulmonary function (FEV1% pred, FVC% pred, MEF% pred, MEF25% pred and MEF50% pred).
Conclusions:
Increased sputum ITGB5 in asthma was positively associated with inflammatory mediators and negatively correlated with pulmonary function, suggesting that ITGB5 upregulation may be involved in airway inflammation and obstruction in asthma pathogenesis.
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