**6. Conclusions**

The definition of eosinophilic asthma engages different models according to different contests [92]. However, a single common thread can be glimpsed in the ability of eosinophils to catch biological and clinical features that are crucial in each contest. Mouse and human allergic asthma models teach us that as the eosinophilic cascade can be dominant after acute exposition to triggers but only within the chronic stimulation, it contributes to deeper structural changes of the airways [11, 17]. The role of eosinophils in different phases of allergic asthma as well as the involving of Th2 cells, cytokines including IL5, IL4 and IL13 and chemokines has been smartly showed in the majority of the experimental studies. In addition, the mechanisms leading to AHR or persistent inflammation imply the need of sharing of different pathways of the Th2 cascade and the cross-talk between eosinophils and other immune cells [41]. The contribution of either IL-5–independent ways or the regulation of local or systemic eosinophilopoiesis has been addressed [40]. In real life, these phenomena can explain the ability of eosinophilic inflammation to be controlled by corticosteroid treatments, and, under certain circumstances, it becomes insensitive to this treatment.

Accordingly, in the context of severe asthma, eosinophilic airway inflammation becomes exceptionally deregulated and needs a biological approach to be controlled. The eosinophilic phenotype of asthma is currently defined by sputum examination that reveals eosinophilic airway inflammation. Generally, eosinophilic subtype of asthma may be defined as symptomatic asthma in the presence of airway eosinophilia and that is characterized by a good response to glucocorticosteroids. The efficacy of reducing exacerbations when corticosteroid treatment was guided according to the sputum eosinophils has addressed the point of eosinophilic target therapy in a subgroup of patients who encounter worse asthma control, higher use of healthcare resources, higher risk of exacerbations and the need of high-dose ICS or systemic corticosteroid treatment to be controlled. Continuous or bust oral corticosteroid exposure is associated to significant adverse effects that significantly impact on the patients' outcome [66], highlighting the urgent need of sparing corticosteroid approaches. Even if limits in accuracy have been evidenced, blood eosinophils can be used in the clinic for detecting airway eosinophilia in uncontrolled severe asthma [78] and as eligibility criteria for anti–IL-5 target therapy. Therefore, new add-on therapies for severe asthma have showed to reduce both asthma exacerbation rate compared to standard of care and daily OCS use. Five biologicals have been now approved for severe eosinophilic asthma and can be applied depending on asthma phenotype and endotype [93]. As a consequence, the precision medicine and personalized therapy have become the best clue for treatment and monitoring the response by identification of suitable biomarkers in patients with more severe and refractory forms of asthma [94].

**145**

**Author details**

Guida Giuseppe\* and Antonelli Andrea

provided the original work is properly cited.

Allergy and Pneumology Unit, A.S.O Santa Croce and Carle, Cuneo, Italy

© 2020 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

\*Address all correspondence to: giuseppe.alesgui@gmail.com

*Eosinophilic Phenotype: The Lesson from Research Models to Severe Asthma*

*DOI: http://dx.doi.org/10.5772/intechopen.92123*

*Eosinophilic Phenotype: The Lesson from Research Models to Severe Asthma DOI: http://dx.doi.org/10.5772/intechopen.92123*

*Cells of the Immune System*

becomes insensitive to this treatment.

and refractory forms of asthma [94].

The definition of eosinophilic asthma engages different models according to different contests [92]. However, a single common thread can be glimpsed in the ability of eosinophils to catch biological and clinical features that are crucial in each contest. Mouse and human allergic asthma models teach us that as the eosinophilic cascade can be dominant after acute exposition to triggers but only within the chronic stimulation, it contributes to deeper structural changes of the airways [11, 17]. The role of eosinophils in different phases of allergic asthma as well as the involving of Th2 cells, cytokines including IL5, IL4 and IL13 and chemokines has been smartly showed in the majority of the experimental studies. In addition, the mechanisms leading to AHR or persistent inflammation imply the need of sharing of different pathways of the Th2 cascade and the cross-talk between eosinophils and other immune cells [41]. The contribution of either IL-5–independent ways or the regulation of local or systemic eosinophilopoiesis has been addressed [40]. In real life, these phenomena can explain the ability of eosinophilic inflammation to be controlled by corticosteroid treatments, and, under certain circumstances, it

Accordingly, in the context of severe asthma, eosinophilic airway inflammation becomes exceptionally deregulated and needs a biological approach to be controlled. The eosinophilic phenotype of asthma is currently defined by sputum examination that reveals eosinophilic airway inflammation. Generally, eosinophilic subtype of asthma may be defined as symptomatic asthma in the presence of airway eosinophilia and that is characterized by a good response to glucocorticosteroids. The efficacy of reducing exacerbations when corticosteroid treatment was guided according to the sputum eosinophils has addressed the point of eosinophilic target therapy in a subgroup of patients who encounter worse asthma control, higher use of healthcare resources, higher risk of exacerbations and the need of high-dose ICS or systemic corticosteroid treatment to be controlled. Continuous or bust oral corticosteroid exposure is associated to significant adverse effects that significantly impact on the patients' outcome [66], highlighting the urgent need of sparing corticosteroid approaches. Even if limits in accuracy have been evidenced, blood eosinophils can be used in the clinic for detecting airway eosinophilia in uncontrolled severe asthma [78] and as eligibility criteria for anti–IL-5 target therapy. Therefore, new add-on therapies for severe asthma have showed to reduce both asthma exacerbation rate compared to standard of care and daily OCS use. Five biologicals have been now approved for severe eosinophilic asthma and can be applied depending on asthma phenotype and endotype [93]. As a consequence, the precision medicine and personalized therapy have become the best clue for treatment and monitoring the response by identification of suitable biomarkers in patients with more severe

**6. Conclusions**

**144**
