<b>Expert opinion</b>: IL-5 antagonism has paved the way for an additional personalized therapeutic opportunity for use in severe asthma with eosinophilic inflammation, though there is limited evidence on the long-term implications of suppressing/depleting eosinophils and the duration for which they should be administered.
<b>Introduction</b>: The precision medicine approach that is now mandatory for severe asthma management includes the use of novel biologic agents blocking specific immunological mechanisms that are responsible for disease phenotypes and endotypes: monoclonal antibodies blocking IgE, IL-5 and IL-4/IL-13 immunological pathways are so far available.
IL-5 mRNA was expressed in PBMC from 2 of 13 patients with asthma, 1 patient with chronic eosinophilic pneumonia, and 1 of 2 patients with idiopathic eosinophilia.
IL-5 levels were higher in induced sputum from patients with asthma and AR compared with nonatopic subjects (p = 0.020 and p = 0.032, respectively), but IFN-gamma levels showed no significant difference between the groups.
Interleukin-5 (IL-5) is involved in the pathophysiology of the disease and drugs targeting IL-5 have been studied for years as a possible treatment option for severe asthma.
A more detailed analysis of the immunological mechanisms underlying the pathogenesis of asthma shows interleukin 5 (IL-5) to be a crucial cytokine in several asthma phenotypes.
All these IL-5 target drugs have been shown to reduce the number of exacerbation in patients with severe asthma selected on the basis of peripheral blood eosinophil count.
Although these pathognomonic features are mainly mediated by antigen-specific Th2 cells and their cytokines, such as IL-4, IL-5, and IL-13, recent studies have revealed that other inflammatory cells, including Th17 cells and innate lymphoid cells (ILCs), also play a critical role in the pathogenesis of asthma.
An animal model of asthma demonstrated that C 1 not only decreased the production of serum IgE and IgG1, and inhibited the production of IL-4 and IL-5 in the bronchoalveolar lavage fluid (BALF).
An early innate response underlies severe influenza-induced exacerbations of asthma in a novel steroid-insensitive and anti-IL-5-responsive mouse model.
An mAb directed against IgE (omalizumab) has become an established add-on therapy for patients with uncontrolled allergic asthma and mAbs specific for IL-5 (reslizumab, mepolizumab), IL-5R (benralizumab), and IL-4R (dupilumab) have been approved as add-on treatments for uncontrolled eosinophilic (type 2) asthma.
Anti-interleukin (IL)-5 mAbs mepolizumab, benralizumab and reslizumab block the interaction between IL-5 and its receptor on eosinophils, thus targeting the eosinophilic pathway in asthma.
Asthma is generally associated with Th2 cells, which produce a panel of cytokines (IL-4, IL-5, IL-13) that act in synergy to drive lung inflammatory responses, mucus secretion, IgE production, and fibrosis, causing the characteristic symptoms of asthma.