**1. Introduction**

Asthma and chronic rhinosinusitis (CRS) are chronic inflammatory disorders involving the lower and upper airways. According to the definition by Global Initiative for Asthma (GINA) documents, asthma is a heterogeneous disease characterized by chronic airway inflammation associated with a history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough and evidence of variable expiratory airflow limitation [1]. Airway inflammation is usually present and persists even when symptoms are absent or lung function is normal.

In the last decades, the role of chronic airway inflammation has been central in the definition of asthma that was recognized as a chronic inflammatory disorder in which many cells and cellular mediators play a role and result in the characteristic pathophysiological changes [2]. The inflammation involves all the airways from the main bronchi to the peripheral small airways. A characteristic pattern of inflammation has been described in asthma involving inflammatory cells mainly mast cells, eosinophils, T lymphocytes, dendritic cells, macrophages and neutrophils, which release mediators that induce symptoms. Both animal models and analysis from human samples have contributed to elucidate the type of inflammation involved in asthma [3]. The most common phenotype of asthma is characterized by eosinophilic airway inflammation and the role of eosinophils as a key player in the pathophysiology of asthma is well documented. Eosinophils emerged as leading cells from the first post-mortem studies of asthmatic lungs, passing through the finding of increased in number and activation status of eosinophils in asthmatic airways [4] and of increased eosinophil surrogates as fractional exhaled nitric oxide (FENO) [5]. Nowadays, the focus is on the definition of the forms of uncontrolled or severe eosinophilic asthma in which airways, sputum and blood eosinophils are consistently increased and represent a biomarker of the eosinophilic endotype of asthma and a guide for biologic target therapies [6, 7].
