Markers and metabolites related to inflammation in bronchiectasis with airflow limitation vs. chronic obstructive pulmonary disease

Abstract

Chronic obstructive pulmonary disease (COPD) is a systemic progressive inflammatory disease resulting from an abnormal inflammatory response to noxious stimuli. Bronchiectasis is also a chronic inflammatory condition, usually caused by repetitive infections. However, it is not clear whether the inflammatory signaling pathways involved are the same in both diseases. Therefore, we here compared the markers and metabolites related to inflammation in COPD and in bronchiectasis to elucidate the pathological mechanisms. We compared markers and metabolites in patients with COPD and in those with bronchiectasis with airflow limitation. The levels of the following inflammatory biomarkers were assessed: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), interleukin (IL)-6, and club cell secretory protein (CC)-16. Additionally, high-resolution metabolomic evaluation was conducted to evaluate the differentially expressed metabolic signature of the two diseases. The ESR and CRP levels were significantly higher, and the levels of CC-16 and IL-6 tended to be higher, among patients with bronchiectasis than among those with COPD. In the metabolomics analysis, serum metabolites of biliverdin IX alpha (m/z: 565.24 [M+H-H2O]+) and L-carnitine (m/z: 184.09 [M+Na]+) were significantly upregulated in sera of bronchiectasis patients. In sera of COPD patients, the levels of nicotine (m/z: 163.12 [M+H]+) and N-acetyl serotonin (m/z: 201.102 [M+H-H2O]+) were significantly higher. Patients with bronchiectasis with airflow limitation had higher levels of inflammatory biomarkers (ESR and CRP) and markers indicating compensation for inflammatory damage (biliverdin IX alpha and L-carnitine), than did patients with COPD. Further treatments modulating the inflammatory process may be useful in patients with bronchiectasis.