Inflammatory and Oxidative Stress Biomarkers in Bronchiectasis:Current Evidence and Future Perspectives—A Review

Abstract

It is a heterogeneous chronic airway disease with an inflammatory cycle of persistent infection with impaired mucociliary clearance, dysregulated host immunity and structural airway damage. Biomarkers can offer a biological dimension of information that enhances the clinical, microbiology, pulmonary function and radiology information. The aim of this review is to emphasis the current evidence on inflammatory and oxidative stress biomarkers in bronchiectasis, including their biological compartments, association with clinical parameters, potential limitations and uses in precision medicine. The most well-established biological process is the neutrophil dominated inflammation, which is represented by the presence of neutrophil extracellular traps, sputum myeloperoxidase, myeloperoxidase, matrix metalloproteinases and inflammatory cytokines in the sputum [1–4,8–12]. Systemic markers such as C-Reactive protein and fibrinogen could be useful to obtain a readily available measure of disease activity and risk of exacerbation but are not specific [13–16]. Oxidative stress can also be measured, by increases in lipid peroxidation and ROS production and decreases in antioxidant defenses [21,22]. Notably, type 2 inflammatory and eosinophilic endotypes have been identified in a clinically meaningful proportion and neutrophilic markers are not able to represent bronchiectasis [28,29]. New proteomic, microbiome, transcriptomic, and composite biomarker approaches might prove to be more effective for endotyping and treatment selection [30–35]. Further studies are warranted including: longitudinal validation, standard assays, clinically relevant thresholds and combining biomarkers with treatable traits (rather than using laboratory assays alone).