학술논문
담배연기에 의한 선천성 면역반응 자극 및 천식의 발생과 악화
Cigarette smoke extract contributes to the inception and aggravation of asthmatic inflammation by stimulating innate immunity
Cigarette smoke extract contributes to the inception and aggravation of asthmatic inflammation by stimulating innate immunity
Document Type
Article
Author
김유진 / Yujin Kim; 김정현 / Jeonghyeon Kim; 모요셉 / Yosep Mo; 박다은 / Da Eun Park; 이현승 / Hyun-seung Lee; 정재우 / Jae-woo Jung; 강혜련 / Hye-ryun Kang
Source
Allergy asthma & respiratory disease. Jul 30, 2022 10(3):145
Subject
Language
Korean
ISSN
2288-0402
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. (Allergy Asthma Respir Dis 2022;10:145-152)