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J Asthma Allergy. 2018 Oct 29;11:267-281. doi: 10.2147/JAA.S153097. eCollection 2018.

Non-eosinophilic asthma: current perspectives.

Author information

1
Department of Allergy, Hospital General de Villalba, Madrid, Spain, igestebang@gmail.com.
2
Department of Allergy, Hospital Universitario Ramón y Cajal (IRYCIS), Madrid, Spain.
3
Department of Allergy, Hospital La Paz Institute for Health Research (IdiPAZ).
4
CIBER de Enfermedades Respiratorias, CIBERES, Madrid, Spain.

Abstract

Although non-eosinophilic asthma (NEA) is not the best known and most prevalent asthma phenotype, its importance cannot be underestimated. NEA is characterized by airway inflammation with the absence of eosinophils, subsequent to activation of non-predominant type 2 immunologic pathways. This phenotype, which possibly includes several not well-defined subphenotypes, is defined by an eosinophil count <2% in sputum. NEA has been associated with environmental and/or host factors, such as smoking cigarettes, pollution, work-related agents, infections, and obesity. These risk factors, alone or in conjunction, can activate specific cellular and molecular pathways leading to non-type 2 inflammation. The most relevant clinical trait of NEA is its poor response to standard asthma treatments, especially to inhaled corticosteroids, leading to a higher severity of disease and to difficult-to-control asthma. Indeed, NEA constitutes about 50% of severe asthma cases. Since most current and forthcoming biologic therapies specifically target type 2 asthma phenotypes, such as uncontrolled severe eosinophilic or allergic asthma, there is a dramatic lack of effective treatments for uncontrolled non-type 2 asthma. Research efforts are now focusing on elucidating the phenotypes underlying the non-type 2 asthma, and several studies are being conducted with new drugs and biologics aiming to develop effective strategies for this type of asthma, and various immunologic pathways are being scrutinized to optimize efficacy and to abolish possible adverse effects.

KEYWORDS:

asthma; asthma endotype; asthma phenotype; neutrophilic asthma; non-eosinophilic asthma

Conflict of interest statement

Disclosure IEG has received lecture fees from Chiesi, Leti, Shire, and Allergy Therapuetics. DA has received lecture fees from Chiesi, Novartis, GSK, Leti, ALK, and AstraZeneca and has served as a consultant to Merck. JD has served as a consultant to LETI, Mundipharma, and GSK and has received lecture fees from Chiesi, Novartis, Leti, AstraZeneca, Stallergenes, and TEVA. SQ has served as a consultant to AstraZeneca, Novartis, Sanofi, Gennetech, Teva, ALK, Mundipharma, and GSK and has received lecture fees from Chiesi, Novartis, Leti, AstraZeneca, Mundipharma, and GSK. The authors report no other conflicts of interest in this work.

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