**3.4 Phenotypes and response to corticosteroids with bronchodilators**

COPD with peripheral blood eosinophilia may have a particularly favorable response to inhaled corticosteroid (ICS)/long-acting β2-adrenergic agonist (LABA) therapy, perhaps because of the inflammation profiling that responds well to corticosteroids. However, prospective studies are required to evaluate the role of blood

*New Perspectives in Pharmacological Therapy for COPD: Phenotype Classification and… DOI: http://dx.doi.org/10.5772/intechopen.106949*


#### **Table 1.**

*Effects of airway eosinophilia and airway hyperresponsiveness as treatable traits on the management of COPD. Illustrated based on refs. [12, 55].*

eosinophils as a biomarker of inhaled therapy response in COPD [110]. Eosinophil counts in the peripheral blood are not always associated with those in the airways. For this reason, patients with COPD who have sputum eosinophilia were enrolled to examine involvement of eosinophilic inflammation in response to corticosteroids and LABA [12, 55, 105, 106]. Inhaled indacaterol (a LABA) caused a greater increase in FEV1 [107] and IC [108] in these patients than those shown in other previous reports. Addition of inhaled ciclesonide (a corticosteroid) to indacaterol caused much higher increases in FEV1 and IC, and values of CAT score and frequency of on demand use of procaterol (a short-acting β2-adrenergic agonist) were markedly reduced (**Table 1**) [12]. These results indicate that not only ICS but also LABA is effective in improving lung function, symptoms, and quality of life in COPD with airway eosinophilia [109]. Since airway inflammation induced by neutrophils and oxidative stress may be the main pathogenesis of COPD, ICS is generally considered to be not so beneficial to this disease. However, ICS/LABA is beneficial to airway eosinophilic inflammation in COPD, similar to that in asthma. Indacaterol, a strong partial β2-adrenergic agonist, is probably effective for COPD because of higher values of its intrinsic efficacy close to a full agonist [111–115]. In these patients with COPD who have sputum eosinophilia, there was no deference in response to indacaterol for FEV1 and IC between these subjects with and without AHR; in contrast, addition to ciclesonide caused greater increases in FEV1 and IC in these subjects without AHR than in these subjects with AHR [12]. However, mechanisms underlining this reduced responsiveness to corticosteroids in COPD with AHR have not been investigated in detail. Therefore, airway eosinophilia and AHR affect symptom suitability (exacerbations) and responsiveness to corticosteroids and β2-adrenergic agonists in COPD (**Table 1**, **Figure 2**).
