Eosinophils play a key role in airway inflammation in many diseases, such as allergic and non-allergic asthma, chronic rhinosinusitis with nasal polyps, and chronic obstructive pulmonary disease. In these chronic disabling conditions, eosinophils contribute to tissue damage, repair, remodeling, and disease persistence through the production a variety of mediators. With the introduction of biological drugs for the treatment of these respiratory diseases, the classification of patients based on clinical characteristics (phenotype) and pathobiological mechanisms (endotype) has become mandatory. This need is particularly evident in severe asthma, where, despite the great scientific efforts to understand the immunological pathways underlying clinical phenotypes, the identification of specific biomarkers defining endotypes or predicting pharmacological response remains unsatisfied. In addition, a significant heterogeneity also exists among patients with other airway diseases. In this review, we describe some of the immunological differences in eosinophilic airway inflammation associated with severe asthma and other airway diseases and how these factors might influence the clinical presentation, with the aim of clarifying when eosinophils play a key pathogenic role and, therefore, represent the preferred therapeutic target.

Eosinophilic Airway Diseases: From Pathophysiological Mechanisms to Clinical Practice / Mormile, Mauro; Mormile, Ilaria; Fuschillo, Salvatore; Rossi, FRANCESCA WANDA; Lamagna, Laura; Ambrosino, Pasquale; DE PAULIS, Amato; Maniscalco, Mauro. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 24:8(2023), p. 7254. [10.3390/ijms24087254]

Eosinophilic Airway Diseases: From Pathophysiological Mechanisms to Clinical Practice

Mauro Mormile;Ilaria Mormile;Francesca Wanda Rossi;Laura Lamagna;Pasquale Ambrosino;Amato de Paulis;Mauro Maniscalco
2023

Abstract

Eosinophils play a key role in airway inflammation in many diseases, such as allergic and non-allergic asthma, chronic rhinosinusitis with nasal polyps, and chronic obstructive pulmonary disease. In these chronic disabling conditions, eosinophils contribute to tissue damage, repair, remodeling, and disease persistence through the production a variety of mediators. With the introduction of biological drugs for the treatment of these respiratory diseases, the classification of patients based on clinical characteristics (phenotype) and pathobiological mechanisms (endotype) has become mandatory. This need is particularly evident in severe asthma, where, despite the great scientific efforts to understand the immunological pathways underlying clinical phenotypes, the identification of specific biomarkers defining endotypes or predicting pharmacological response remains unsatisfied. In addition, a significant heterogeneity also exists among patients with other airway diseases. In this review, we describe some of the immunological differences in eosinophilic airway inflammation associated with severe asthma and other airway diseases and how these factors might influence the clinical presentation, with the aim of clarifying when eosinophils play a key pathogenic role and, therefore, represent the preferred therapeutic target.
2023
Eosinophilic Airway Diseases: From Pathophysiological Mechanisms to Clinical Practice / Mormile, Mauro; Mormile, Ilaria; Fuschillo, Salvatore; Rossi, FRANCESCA WANDA; Lamagna, Laura; Ambrosino, Pasquale; DE PAULIS, Amato; Maniscalco, Mauro. - In: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES. - ISSN 1422-0067. - 24:8(2023), p. 7254. [10.3390/ijms24087254]
File in questo prodotto:
File Dimensione Formato  
ijms-24-07254.pdf

accesso aperto

Licenza: Dominio pubblico
Dimensione 1.26 MB
Formato Adobe PDF
1.26 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11588/922965
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus 7
  • ???jsp.display-item.citation.isi??? 6
social impact