Increased chemokines levels in patients with chronic obstructive pulmonary disease: correlation with quantitative computed tomography metrics.

Objective: We sought to explore the relationships between multiple chemokines with spirometry, inflammatory mediators and CT findings of emphysema, small airways disease and bronchial wall thickness.

Methods: All patients with COPD ( = 65) and healthy control subjects ( = 23) underwent high-resolution CT, with image analysis determining the low attenuation area (LAA), ratio of mean lung attenuation on expiratory and inspiratory scans (E/I MLD) and bronchial wall thickness of inner perimeter of a 10-mm diameter airway (Pi10). At enrollment, subjects underwent pulmonary function studies, chemokines and inflammatory mediators measurements.

Results: Multiple chemokines (CCL2, CCL3, CCL5, CX3CL1, CXCL8, CXCL9, CXCL10, CXCL11 and CXCL12) and inflammatory mediators (MMP-9, MMP-12, IL-18 and neutrophil count) were markedly increased in the serum of COPD patients compared with healthy controls. There were associations between small airway disease (E/I MLD) and CCL11, CXCL8, CXCL10, CXCL11, CXCL12 and CX3CL1. Especially CXCL8 and CX3CL1 are strongly associated with E/I MLD ( = 0.74, < 0.001; = 0.76, < 0.001, respectively). CXCL8, CXCL12 and CX3CL1 were moderately positively correlated with emphysema (%LAA) ( = 0.49, < 0.05; = 0.51, < 0.05; = 0.54, < 0.01, respectively). Bronchial wall thickness (Pi10）showed no significant differences between the COPD and healthy controls,，but there was an association between Pi10 and FEV% in COPD patients (r=-0.420, = 0.048). Our statistical results showed that there were not any associations between airway wall thickness (Pi10) and chemokines.

Conclusion: Pulmonary chemokines levels are closely associated with the extent of gas trapping, small airways disease and emphysema identified on high-resolution chest CT scan.

Advances In Knowledge: This study combines quantitative CT analysis with multiplex chemokines and inflammatory mediators to identify a new role of pathological changes in COPD.