Metabolomics in the Identification of Biomarkers of Asthma.

Abstract

Asthma is a major non-communicable disease characterized by recurrent attacks of breathlessness and wheezing. According to World Health Organization (WHO), it is estimated that more than 339 million people had asthma globally in 2016. Indeed, there were 417,918 deaths, due to asthma at the global level. The concept of asthma as a single entity has now evolved into a much more complex biological network of distinct and interrelating inflammatory pathways. Asthma is considered a multifactorial, chronic syndrome, which varies over time and involves genetic and environmental interactions. It causes reversible airway obstruction through spasm, inflammation, and hypersecretion associated with airway hyperresponsiveness (AHR), inf iltration of immune cells into the airway submucosa, and airway epithelial remodeling [1]. This heterogeneity reflects the underlying mechanisms (endotypes) and variable clinical presentations (phenotypes) [2]. The inflammatory phenotypes identified to date include eosinophilic or T2 or T2-high asthma, and non-eosinophilic, non-T2 or T2-low asthma, which comprises, in turn, the neutrophilic and paucigranulocytic phenotypes. Another level of complexity resides because even with similar clinical symptoms, patients may respond differently to the same therapeutic interventions [3].