담배연기에 의한 선천성 면역반응 자극 및 천식의 발생과 악화open accessCigarette smoke extract contributes to the inception and aggravation of asthmatic inflammation by stimulating innate immunity
- Authors
- 김유진; 김정현; 모요셉; 박다은; 이현승; 정재우; 강혜련
- Issue Date
- Jul-2022
- Publisher
- 대한 소아알레르기 호흡기학회
- Keywords
- Asthma; Cigarette smoking; Innate Immunity; Macrophages; .
- Citation
- Allergy Asthma & Respiratory Diseases, v.10, no.3, pp 145 - 152
- Pages
- 8
- Journal Title
- Allergy Asthma & Respiratory Diseases
- Volume
- 10
- Number
- 3
- Start Page
- 145
- End Page
- 152
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/71212
- DOI
- 10.4168/aard.2022.10.3.145
- ISSN
- 2288-0402
2288-0410
- 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.
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