title: Neutrophilic inflammation in asthma: mechanisms and therapeutic considerations.
abstract: Neutrophilic airway inflammation represents a pathologically distinct form of asthma and frequently appears in symptomatic adulthood asthmatics. However, clinical impacts and mechanisms of the neutrophilic inflammation have not been thoroughly evaluated up to date. Areas covered: Currently, distinct clinical manifestations, triggers, and molecular mechanisms of the neutrophilic inflammation (namely Toll-like receptor, Th1, Th17, inflammasome) are under investigation in asthma. Furthermore, possible role of the neutrophilic inflammation is being investigated in respect to the airway remodeling. We searched the related literatures published during the past 10 years on the website of Pub Med under the title of asthma and neutrophilic inflammation in human. Expert commentary: Epidemiologic and experimental studies have revealed that the neutrophilic airway inflammation is induced by a wide variety of stimuli including ozone, particulate matters, cigarette smoke, occupational irritants, endotoxins, microbial infection and colonization, and aeroallergens. These triggers provoke diverse immune and inflammatory responses leading to progressive and sometimes irreversible airway obstruction. Clinically, neutrophilic airway inflammation is frequently associated with severe asthma and poor response to glucocorticoid therapy, indicating the need for other treatment strategies. Accordingly, therapeutics will be targeted against the main mediators behind the underlying molecular mechanisms of the neutrophilic inflammation.
authors.affiliation: a Department of Interdisciplinary Program in Biomedical Science Major , Soonchunhyang Graduate School , Bucheon , Gyeonggi-do , Republic of Korea.
authors.forename: Hun Soo
authors.initials: HS
authors.lastname: Chang
authors.affiliation: a Department of Interdisciplinary Program in Biomedical Science Major , Soonchunhyang Graduate School , Bucheon , Gyeonggi-do , Republic of Korea.
authors.forename: Tae-Hyeong
authors.initials: TH
authors.lastname: Lee
authors.affiliation: a Department of Interdisciplinary Program in Biomedical Science Major , Soonchunhyang Graduate School , Bucheon , Gyeonggi-do , Republic of Korea.
authors.forename: Ji Ae
authors.initials: JA
authors.lastname: Jun
authors.affiliation: b Division of Allergy and Respiratory Disease , Soonchunhyang University Bucheon Hospital , Bucheon , Gyeonggi-do , Republic of Korea.
authors.forename: Ae Rin
authors.initials: AR
authors.lastname: Baek
authors.affiliation: b Division of Allergy and Respiratory Disease , Soonchunhyang University Bucheon Hospital , Bucheon , Gyeonggi-do , Republic of Korea.
authors.forename: Jong-Sook
authors.initials: JS
authors.lastname: Park
authors.affiliation: c Division of Allergy and Respiratory Medicine , Soonchunhyang University Seoul Hospital , Seoul , Republic of Korea.
authors.forename: So-My
authors.initials: SM
authors.lastname: Koo
authors.affiliation: c Division of Allergy and Respiratory Medicine , Soonchunhyang University Seoul Hospital , Seoul , Republic of Korea.
authors.forename: Yang-Ki
authors.initials: YK
authors.lastname: Kim
authors.affiliation: d Division of Respiratory Medicine , Soonchunhyang University CheonAn Hospital , Cheonan , Chungcheongnam-do , Republic of Korea.
authors.forename: Ho Sung
authors.initials: HS
authors.lastname: Lee
authors.affiliation: b Division of Allergy and Respiratory Disease , Soonchunhyang University Bucheon Hospital , Bucheon , Gyeonggi-do , Republic of Korea.
authors.forename: Choon-Sik
authors.initials: CS
authors.lastname: Park
mesh_terms: D000402:Airway Obstruction / Q000276:immunology*; D056151:Airway Remodeling / Q000276:immunology; D001249:Asthma / Q000276:immunology*; D006801:Humans; D058847:Inflammasomes / Q000276:immunology; D007249:Inflammation / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D012137:Respiratory System / Q000276:immunology; D058504:Th17 Cells / Q000276:immunology
chemical_list: D058847:Inflammasomes
keywords: Asthma; HRCT; biologics; innate immune response; neutrophilc inflammation; remodeling