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Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target

Asthma is a chronic inflammatory disease that undermines the airways. It is caused by dysfunction of various types of cells, as well as cellular components, and is characterized by recruitment of inflammatory cells, bronchial hyperreactivity, mucus production, and airway remodelling and narrowing. I...

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Detalles Bibliográficos
Autores principales: Gao, Han, Ying, Songmin, Dai, Yuanrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735647/
https://www.ncbi.nlm.nih.gov/pubmed/29359169
http://dx.doi.org/10.1155/2017/3743048
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author Gao, Han
Ying, Songmin
Dai, Yuanrong
author_facet Gao, Han
Ying, Songmin
Dai, Yuanrong
author_sort Gao, Han
collection PubMed
description Asthma is a chronic inflammatory disease that undermines the airways. It is caused by dysfunction of various types of cells, as well as cellular components, and is characterized by recruitment of inflammatory cells, bronchial hyperreactivity, mucus production, and airway remodelling and narrowing. It has commonly been considered that airway inflammation is caused by the Th2 immune response, or eosinophilia, which is a hallmark of bronchial asthma pathogenesis. Some patients display a neutrophil-dominant presentation and are characterized with low (or even absent) Th2 cytokines. In recent years, increasing evidence has also suggested that neutrophils play a key role in the development of certain subtypes of asthma. This review discusses neutrophils in asthma and potentially related targeted therapies.
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spelling pubmed-57356472018-01-22 Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target Gao, Han Ying, Songmin Dai, Yuanrong J Immunol Res Review Article Asthma is a chronic inflammatory disease that undermines the airways. It is caused by dysfunction of various types of cells, as well as cellular components, and is characterized by recruitment of inflammatory cells, bronchial hyperreactivity, mucus production, and airway remodelling and narrowing. It has commonly been considered that airway inflammation is caused by the Th2 immune response, or eosinophilia, which is a hallmark of bronchial asthma pathogenesis. Some patients display a neutrophil-dominant presentation and are characterized with low (or even absent) Th2 cytokines. In recent years, increasing evidence has also suggested that neutrophils play a key role in the development of certain subtypes of asthma. This review discusses neutrophils in asthma and potentially related targeted therapies. Hindawi 2017 2017-11-22 /pmc/articles/PMC5735647/ /pubmed/29359169 http://dx.doi.org/10.1155/2017/3743048 Text en Copyright © 2017 Han Gao et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Gao, Han
Ying, Songmin
Dai, Yuanrong
Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target
title Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target
title_full Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target
title_fullStr Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target
title_full_unstemmed Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target
title_short Pathological Roles of Neutrophil-Mediated Inflammation in Asthma and Its Potential for Therapy as a Target
title_sort pathological roles of neutrophil-mediated inflammation in asthma and its potential for therapy as a target
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5735647/
https://www.ncbi.nlm.nih.gov/pubmed/29359169
http://dx.doi.org/10.1155/2017/3743048
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