담배연기에 의한 선천성 면역반응 자극 및 천식의 발생과 악화
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 김유진 | - |
dc.contributor.author | 김정현 | - |
dc.contributor.author | 모요셉 | - |
dc.contributor.author | 박다은 | - |
dc.contributor.author | 이현승 | - |
dc.contributor.author | 정재우 | - |
dc.contributor.author | 강혜련 | - |
dc.date.accessioned | 2024-01-22T01:00:34Z | - |
dc.date.available | 2024-01-22T01:00:34Z | - |
dc.date.issued | 2022-07 | - |
dc.identifier.issn | 2288-0402 | - |
dc.identifier.issn | 2288-0410 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/71212 | - |
dc.description.abstract | Purpose: Smoking is a risk factor for the development of asthma and worsens the long-term prognosis of asthma. This study investigated the effect of cigarette smoke extract (CSE) on innate immune cells such as innate lymphoid cells (ILCs) and macrophages in a murine model of induced asthma. Methods: Six-week-old female BALB/C mice were exposed to ovalbumin (OVA) via an intranasal route with or without CSE for 8 weeks to establish a chronic murine asthma model. Airway hyperresponsiveness (AHR), airway inflammatory cells from bronchoalveolar lavage fluid, and the population of CD4+ T cells, ILCs, and macrophages in the lungs were studied to evaluate the effect of chronic CSE exposure on asthma. Results: Mice intranasally exposed to CSE along with OVA treatment (CSE/OVA) had significantly enhanced AHR, eosinophilic inflammation, increased IL-13 and IL-17 producing CD4+ T cells compared to mice intranasally exposed to OVA only. On the contrary, the frequency of Foxp3+ in CD4+ T cells was reduced in the CSE/OVA group. CSE enhanced the dendritic cell (DC) population, especially MHCII+ DC with antigen-presenting capacity. Among ILCs, the CSE/OVA group showed a significant increase of IL-13-producing type 2 ILCs, but not interferon-γ+ ILC1s and IL-17+ ILC3s. . Among macrophages, alveolar macrophage and Ym-1 and FIZZ1 positive M2 macrophage populations were significantly induced by CSE exposure alone and when combined with OVA treatment. Conclusion: In this study, we showed that long-term exposure to cigarette smoke contributes to the inception and aggravation of asthmatic inflammation by enhancing DCs, ILC2, and M2 alveolar macrophage populations in the mouse model. | - |
dc.format.extent | 8 | - |
dc.language | 한국어 | - |
dc.language.iso | KOR | - |
dc.publisher | 대한 소아알레르기 호흡기학회 | - |
dc.title | 담배연기에 의한 선천성 면역반응 자극 및 천식의 발생과 악화 | - |
dc.title.alternative | Cigarette smoke extract contributes to the inception and aggravation of asthmatic inflammation by stimulating innate immunity | - |
dc.type | Article | - |
dc.identifier.doi | 10.4168/aard.2022.10.3.145 | - |
dc.identifier.bibliographicCitation | Allergy Asthma & Respiratory Diseases, v.10, no.3, pp 145 - 152 | - |
dc.identifier.kciid | ART002862967 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.wosid | 000859094200005 | - |
dc.citation.endPage | 152 | - |
dc.citation.number | 3 | - |
dc.citation.startPage | 145 | - |
dc.citation.title | Allergy Asthma & Respiratory Diseases | - |
dc.citation.volume | 10 | - |
dc.type.docType | Article | - |
dc.publisher.location | 대한민국 | - |
dc.subject.keywordAuthor | Asthma | - |
dc.subject.keywordAuthor | Cigarette smoking | - |
dc.subject.keywordAuthor | Innate Immunity | - |
dc.subject.keywordAuthor | Macrophages | - |
dc.subject.keywordAuthor | . | - |
dc.subject.keywordPlus | LYMPHOID-CELLS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | PLASTICITY | - |
dc.subject.keywordPlus | ADJUVANT | - |
dc.subject.keywordPlus | IL-17A | - |
dc.subject.keywordPlus | COPD | - |
dc.relation.journalResearchArea | Allergy | - |
dc.relation.journalWebOfScienceCategory | Allergy | - |
dc.description.journalRegisteredClass | esci | - |
dc.description.journalRegisteredClass | kci | - |
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