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.