2. Role of the airway epithelium in initiating asthma phenotypes:
In 2009 the global initiative for asthma (GINA) proposed the concept of asthma phenotypes. Current research on asthma phenotypes mainly focus on two aspects namely different inflammatory phenotypes and how they may link to previously described clinical phenotypes [22]. Inflammatory phenotypes are based on the type of granulocytic cells present in induced sputum and is divided into eosinophilic, neutrophilic, mixed granulocytic and pauci-granulocytic of which eosinophilic type is the most common. Clinical phenotyping uses multiple clinical variables including age, gender, age of onset, BMI, symptoms, atopic status, and lung function tests to cluster patients [22]. More recently, there have been combined approaches undertaken whereby the gene expression profiles determine whether specific genes or pathways are associated with clinical phenotypes [23].
There are many types of clinical phenotypes and GINA lists some of the most common phenotypes including allergic, non-allergic, late-onset, fixed airflow limitation and obese asthma [https://ginasthma.org/ ]. Additional asthma endotypes have also been proposed reflecting increased knowledge regarding asthma pathogenesis. However, these endotypes are still be broadly regarded as either type 2-high (T2high) and type 2-low (T2low) [24]. It is evident that the current status of asthma phenotypes and endotypes is complex with overlaps and subtypes present. This may reflect the following problems: (1) The evaluation standards adopted by researchers are different, and the conclusions drawn are also very different, so that there is no unified standard. (2) Asthma phenotypes sometimes overlap, which makes it difficult to distinctly classify affected patients [25]. (3) The use of cross-sectional data that does not indicate stability over time or with treatment. (4) The impact of respiratory tract infections and allergen exposures on the airway inflammation phenotype.