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Updated: Nov 18, 2025

Methodology for Sputum Induction and Laboratory Processing
Published on: December 17, 2017
Elevated sputum IL-36 levels are associated with neutrophil-related inflammation in COPD patients
Wei Li1, Xiaoli Meng1, Yuqiu Hao1
1Department of Respiratory and Critical Care Medicine, the Second Hospital of Jilin University, Changchun, Jilin, 130041, China.
Background:
Interleukin (IL)-36, including IL-36α, IL-36β, and IL-36γ in the IL-1 family, are agonists of their receptors. IL-36 expression is associated with inflammation, including lung infection in humans. However, there is no information on its role in the inflammation of different types of chronic obstructive pulmonary disease (COPD).
Objective:
This study focused on the sputum IL-36α, IL-36β, and IL-36γ levels in stable COPD patients and their relationship with lung function and other cytokines in different inflammatory types of COPD patients.
Methods:
Sputum specimens were collected from 73 stable COPD patients and 20 age- and gender-matched healthy controls. The levels of sputum IL-36α, IL-36β, and IL-36γ and other cytokines were quantified and sputum cells were characterized. The potential relationship between the levels of sputum IL-36α, IL-36β, or IL-36γ and lung functional measures, inflammatory cells, and cytokines was analyzed.
Results:
In comparison with the healthy controls, sputum IL-36α and IL-36γ levels significantly increased in COPD (106.8 pg/mL vs. 76.9 pg/mL P =.001, 397.9 pg/mL vs. 359.5 pg/mL P =.006). The sputum IL-36α and IL-36γ levels were significantly higher in the neutrophilic and mixed granulocytic types than that in the eosinophilic and paucigranulocytic types of COPD patients. The sputum IL-36α levels were positively correlated with sputum IL-36γ levels and the numbers of sputum neutrophils, and the sputum IL-36γ levels were positively correlated with the numbers of sputum lymphocytes in COPD patients.
Conclusions:
Elevated levels of sputum IL-36α and IL-36γ were detected in COPD patients and may provide insights into the inflammatory pathways in neutrophilic COPD.
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