Updated biomarkers for extracellular traps from neutrophil, monocyte, and M1 macrophage in neutrophilic asthma: a narrative review
Abstract
Asthma, a common chronic inflammatory condition in the airways, significantly impacts individuals across all age groups and poses a substantial global health burden. Despite the availability of conventional treatments, a considerable proportion of asthmatic patients continue to experience uncontrolled asthma symptoms. This review focuses on neutrophilic asthma (NA), a challenging endotype characterized by lower lung function, a higher frequency of symptom exacerbations, and a poorer response to standard therapies. NA is typically diagnosed by an increase presence of airway neutrophils, as identified by sputum profile analysis. However, this method is not always available in resource-limited settings. Therefore, NA remains a public health concern that is still under-researched and under-diagnosed. Immune cell activation and their extracellular traps (ETs) could initiate the inflammatory signaling pathways, resulting in airway damage in asthma. These ETs released significant quantities of extracellular DNA, a process governed by the cytokines interleukin (IL)-8 and tumor necrosis factor-alpha. As a result, several investigations have identified these molecules as established biomarkers and explored therapies desinged to modulate neutrophil ETs (NETs), monocyte ETs (MoETs), and M1 macrophage ETs (M1ETs). Recent findings indicate that C-C motif chemokine ligand 4 like 2, calcium-binding protein A9, serum amyloid A1, and IL-1β promote NET formation, whereas monocyte chemoattractant protein-1 and soluble regulation of tumorigenicity 2 are essential components of MoETs and M1ETs. Therefore, these biomarkers are emerging as predictors for NETs, MoETs, and M1ETs. This review aims to discuss the pathophysiology, diagnostic criteria, and treatment options for NA, emphasizing the role of NETs, MoETs, and M1ETs in exacerbating airway inflammation.
