Asthma and
chronic obstructive pulmonary disease (
COPD) are chronic inflammatory diseases of the airway, although the drivers and site of the
inflammation differ between diseases. Asthmatics with a neutrophilic airway
inflammation are associated with a poor response to
corticosteroids, whereas asthmatics with eosinophilic
inflammation respond better to
corticosteroids.
Biologicals targeting the Th2-eosinophil
nexus such as anti-
interleukin (IL)-4, anti-IL-5, and anti-IL-13 are ineffective in
asthma as a whole but are more effective if patients are selected using cellular (eg, eosinophils) or molecular (eg,
periostin)
biomarkers. This highlights the key role of individual inflammatory mediators in driving the inflammatory response and for accurate disease phenotyping to allow greater understanding of disease and development of patient-oriented antiasthma
therapies. In contrast to asthmatic patients,
corticosteroids are relatively ineffective in
COPD patients. Despite stratification of
COPD patients, the results of targeted
therapy have proved disappointing with the exception of recent studies using
CXC chemokine receptor (CXCR)2 antagonists. Currently, several other novel mediator-targeted drugs are undergoing clinical trials. As with
asthma specifically targeted treatments may be of most benefit in specific
COPD patient endotypes. The use of novel inflammatory mediator-targeted therapeutic agents in selected patients with
asthma or
COPD and the detection of markers of responsiveness or nonresponsiveness will allow a link between clinical phenotypes and pathophysiological mechanisms to be delineated reaching the goal of endotyping patients.