Steroid-Resistant Asthma and Neutrophils

Asthma patients are classified by phenotype and endotype. Although symptoms in most asthma patients are well controlled by glucocorticoid treatment, certain populations of severe eosinophilic asthma patients in T-helper 2 (Th2)/type 2 asthma and neutrophilic asthma patients in non-Th2/type 2 asthma...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2020/01/01, Vol.43(1), pp.31-35
Main Author: Nabe, Takeshi
Format: Article
Language:English
Subjects:
Asthma
Cell death
eosinophil
Glucocorticoids
Helper cells
Inflammation
Interleukin 17
Interleukin 8
Leukocytes (eosinophilic)
Leukocytes (neutrophilic)
Lymphocytes T
Lymphoid cells
Macrophages
NETosis
neutrophil
Neutrophils
Pathogenesis
Phenotypes
Respiratory tract
Respiratory tract diseases
steroid
Steroids
Tumor necrosis factor-α
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Summary:Asthma patients are classified by phenotype and endotype. Although symptoms in most asthma patients are well controlled by glucocorticoid treatment, certain populations of severe eosinophilic asthma patients in T-helper 2 (Th2)/type 2 asthma and neutrophilic asthma patients in non-Th2/type 2 asthma show insensitivity to inhaled or oral glucocorticoid therapy. In some cases of severe eosinophilic asthma, eosinophils remain in the lungs despite glucocorticoid therapy. It was reported that interleukin (IL)-33-induced activation of type 2 innate lymphoid cells (ILC2) was resistant to glucocorticoid treatment in certain allergic conditions. Regarding neutrophilic airway inflammation in steroid-resistant asthma, IL-17 derived from Th17 cells and IL-8 and tumor necrosis factor-α derived mainly from macrophages were reported to be involved in the pathogenesis. Recently, “NETosis,” a specific cell death of neutrophils, has been reported to be involved in asthmatic airway inflammation. When NETosis is induced in asthma, aggravation of inflammation and delay of tissue repair could occur, suggesting that NETosis may be associated with the development of steroid-resistant asthma. This article reviews the pathogenesis of steroid-resistant asthma by focusing mainly on neutrophils.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.b19-00095