한빛사논문
- 조회636
Jongho Ham1,2,10, Jihyun Kim1,3,10, Kyoung-Hee Sohn4, In-Won Park5, Byoung-Whui Choi5,6, Doo Hyun Chung2,7,8, Sang-Heon Cho3,9, Hye Ryun Kang3,9, Jae-Woo Jung5,* & Hye Young Kim1,2,3,*
1Laboratory of Mucosal Immunology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.
2Department of Biomedical Sciences, BK21 Plus Biomedical Science Project, Seoul National University College of Medicine, Seoul, Republic of Korea.
3Institute of Allergy and Clinical Immunology, Seoul National University Medical Research Center, Seoul, South Korea.
4Department of Internal Medicine, Kyung Hee University Medical Center, Seoul, Republic of Korea.
5Department of Internal Medicine, Chung-Ang University College of Medicine, Seoul, South Korea.
6Department of Internal Medicine, Chung-Ang University H.C.S. Hyundae l Hospital, Namyangju, South Korea.
7Department of Pathology, Seoul National University College of Medicine, Seoul, South Korea.
8Laboratory of Immune Regulation, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea.
9Department of Internal Medicine, Seoul National University Hospital, Seoul, South Korea.
10These authors contributed equally: Jongho Ham, Jihyun Kim.
*Corresponding author.
Abstract
Although cigarette smoking is known to exacerbate asthma, only a few clinical asthma studies have been conducted involving smokers. Here we show, by comparing paired sputum and blood samples from smoking and non-smoking patients with asthma, that smoking associates with significantly higher frequencies of pro-inflammatory, natural-cytotoxicity-receptor-non-expressing type 3 innate lymphoid cells (ILC3) in the sputum and memory-like, CD45RO-expressing ILC3s in the blood. These ILC3 frequencies positively correlate with circulating neutrophil counts and M1 alveolar macrophage frequencies, which are known to increase in uncontrolled severe asthma, yet do not correlate with circulating eosinophil frequencies that characterize allergic asthma. In vitro exposure of ILCs to cigarette smoke extract induces expression of the memory marker CD45RO in ILC3s. Cigarette smoke extract also impairs the barrier function of airway epithelial cells and increases their production of IL-1β, which is a known activating factor for ILC3s. Thus, our study suggests that cigarette smoking increases local and circulating frequencies of activated ILC3 cells, plays a role in their activation, thereby aggravating non-allergic inflammation and the severity of asthma.
논문정보
- Research article
- 2022년 07월 (BRIC 등록일 2022-07-22)
- 국내 연구진
- 의약학 > 면역의학
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