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Defining a non-eosinophilic inflammatory subtype in COPD: the role of CXCL9 and type 1 immune responses
Yin Chengsheng1, Song Jiacui1, Takehiro Hasegawa2
1Department of Respiratory Medicine, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China.
Insights
C-X-C motif chemokine ligand 9 (CXCL9) serum levels are elevated in patients with chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD). Higher CXCL9 levels correlate with disease severity markers in COPD, suggesting its role in respiratory inflammation.
Area of Science:
- Immunology
- Pulmonology
- Biochemistry
Background:
- C-X-C motif chemokine ligand 9 (CXCL9) is interferon-γ-induced and a marker for T-helper 1 (Th1) cells.
- CXCL9 expression is elevated in interstitial lung disease (ILD), COVID-19, and asthma.
- The role of Th1 chemokines in chronic obstructive pulmonary disease (COPD) pathophysiology is not fully understood.
Purpose of the Study:
- To investigate the relationship between C-X-C motif chemokine ligand 9 (CXCL9) and chronic respiratory diseases.
- To assess serum CXCL9 levels in patients with COPD and ILD.
Main Methods:
- Retrospective cohort study of 165 patients with ILD and COPD.
- Serum levels of CXCL9, surfactant protein A (SP-A), Krebs von den Lungen-6 (KL-6), and C-reactive protein (CRP) were analyzed.
- Unsupervised hierarchical cluster analysis was performed for data clustering.
Main Results:
- Serum CXCL9 levels were significantly higher in patients with COPD and ILD compared to healthy controls.
- CXCL9 levels in COPD patients correlated with KL-6, SP-A, blood eosinophil ratio, lactate dehydrogenase (LDH), and CRP.
- High CXCL9 levels in non-eosinophilic COPD were associated with elevated LDH, KL-6, and neutrophil ratio.
Conclusions:
- CXCL9 may play a significant role in the inflammatory processes of COPD.
- Elevated CXCL9 levels are associated with specific biomarkers and disease characteristics in COPD.
Background:
C-X-C motif chemokine ligand 9 (CXCL9) is induced by the interferon-γ response, and its receptor, C-X-C motif chemokine receptor 3, is a well-established marker of T-helper 1 (Th1) cells, which play an essential role in type 1 immune responses. CXCL9 expression is upregulated in patients with interstitial lung disease (ILD), COVID-19, and asthma. Although type 1 inflammation and CD8+ T cell activation are considered central to the inflammatory pathophysiology of chronic obstructive pulmonary disease (COPD), the relationship between blood levels of Th1 chemokines and this pathophysiology remains unclear. This study aimed to investigate the relationship between CXCL9 and chronic respiratory diseases.
Methods:
We conducted a retrospective cohort study. The serum levels of CXCL9, surfactant protein A (SP-A), Krebs von den Lungen-6 (KL-6), and C-reactive protein (CRP) were analyzed in 165 patients with ILD and COPD. COPD was diagnosed using pulmonary function tests according to the Global Initiative for Chronic Obstructive Lung Disease criteria. Statistical analyses included Fisher's exact test, Steel-Dwass test, Mann-Whitney U, and Wilcoxon test. An unsupervised hierarchical cluster analysis using complete linkage and Euclidean distance was performed for data clustering.
Results:
CXCL9 levels were significantly higher in patients with COPD and interstitial ILD than in healthy smokers and non-smokers. The median serum CXCL9 levels in patients with ILD, COPD, healthy smokers, and healthy nonsmokers were 61.6, 69.3, 37.0, and 32.5pg/mL, respectively. CXCL9 levels in patients with COPD significantly correlated with KL-6, SP-A, blood eosinophil ratio, lactate dehydrogenase (LDH), and CRP levels, with correlation coefficients of 0.243, 0.381, 0.225, 0.369, and 0.293, respectively. Additionally, CXCL9 levels were negatively correlated with FEV1%. Levels of LDH and KL-6 and the neutrophil ratio were significantly elevated in non-eosinophilic COPD patients with high CXCL9 levels.
Conclusions:
Our results highlight the potential role of CXCL9 in the inflammatory pathophysiology of COPD.
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