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Neutrophilic inflammation in asthma: mechanisms and therapeutic considerations

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dc.contributor.authorChang, Hun Soo-
dc.contributor.authorLee, Tae-Hyeong-
dc.contributor.authorJun, Ji Ae-
dc.contributor.authorBaek, Ae Rin-
dc.contributor.authorPark, Jong-Sook-
dc.contributor.authorKoo, So-My-
dc.contributor.authorKim, Yang-Ki-
dc.contributor.authorLee, Ho Sung-
dc.contributor.authorPark, Choon-Sik-
dc.date.accessioned2021-08-11T16:24:30Z-
dc.date.available2021-08-11T16:24:30Z-
dc.date.issued2017-
dc.identifier.issn1747-6348-
dc.identifier.issn1747-6356-
dc.identifier.urihttps://scholarworks.bwise.kr/sch/handle/2021.sw.sch/8452-
dc.description.abstractIntroduction: 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.-
dc.format.extent12-
dc.language영어-
dc.language.isoENG-
dc.publisherExpert Reviews-
dc.titleNeutrophilic inflammation in asthma: mechanisms and therapeutic considerations-
dc.typeArticle-
dc.publisher.location영국-
dc.identifier.doi10.1080/17476348.2017.1268919-
dc.identifier.scopusid2-s2.0-85006757726-
dc.identifier.wosid000394694400005-
dc.identifier.bibliographicCitationExpert Review of Respiratory Medicine, v.11, no.1, pp 29 - 40-
dc.citation.titleExpert Review of Respiratory Medicine-
dc.citation.volume11-
dc.citation.number1-
dc.citation.startPage29-
dc.citation.endPage40-
dc.type.docTypeReview-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaRespiratory System-
dc.relation.journalWebOfScienceCategoryRespiratory System-
dc.subject.keywordPlusOBSTRUCTIVE PULMONARY-DISEASE-
dc.subject.keywordPlusPERSISTENT AIRWAY-OBSTRUCTION-
dc.subject.keywordPlusPOORLY CONTROLLED ASTHMA-
dc.subject.keywordPlusNON-EOSINOPHILIC ASTHMA-
dc.subject.keywordPlusNECROSIS-FACTOR-ALPHA-
dc.subject.keywordPlusREFRACTORY ASTHMA-
dc.subject.keywordPlusINDUCED SPUTUM-
dc.subject.keywordPlusHEALTHY-VOLUNTEERS-
dc.subject.keywordPlusEPITHELIAL-CELLS-
dc.subject.keywordPlusDOUBLE-BLIND-
dc.subject.keywordAuthorAsthma-
dc.subject.keywordAuthorneutrophilc inflammation-
dc.subject.keywordAuthorbiologics-
dc.subject.keywordAuthorremodeling-
dc.subject.keywordAuthorinnate immune response-
dc.subject.keywordAuthorHRCT-
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