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Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
Published on: April 16, 2019
Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells
Jongho Ham1,2, Jihyun Kim1,3, Kyoung-Hee Sohn4
1Laboratory of Mucosal Immunology, Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, Republic of Korea.
Smoking increases pro-inflammatory innate lymphoid cells (ILC3) in asthma patients. This cellular activation by cigarette smoke exacerbates non-allergic inflammation and asthma severity.
Area of Science:
- Immunology
- Respiratory Medicine
Background:
- Cigarette smoking is a known asthma exacerbator, yet few studies focus on smokers.
- Asthma severity is linked to specific immune cell profiles.
Purpose of the Study:
- To investigate the impact of smoking on immune cell populations in asthma.
- To elucidate the role of innate lymphoid cells (ILC3) in smoking-related asthma exacerbation.
Main Methods:
- Comparison of sputum and blood samples from smoking and non-smoking asthma patients.
- In vitro exposure of innate lymphoid cells (ILCs) to cigarette smoke extract.
- Analysis of ILC3 frequencies, CD45RO expression, neutrophil counts, M1 alveolar macrophages, and airway epithelial barrier function.
Main Results:
- Smoking associated with higher frequencies of pro-inflammatory ILC3s in sputum and memory-like ILC3s in blood.
- ILC3 frequencies correlated with neutrophil counts and M1 alveolar macrophages, not eosinophils.
- Cigarette smoke extract induced CD45RO expression on ILC3s and impaired airway epithelial barrier function, increasing IL-1β production.
Conclusions:
- Cigarette smoking increases local and circulating activated ILC3 frequencies.
- Smoking contributes to ILC3 activation, exacerbating non-allergic asthma inflammation and severity.
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