Journal of Capital Medical University ›› 2016, Vol. 37 ›› Issue (5): 561-567.doi: 10.3969/j.issn.1006-7795.2016.05.001

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Changes of immune cells and their subsets in lungs of interleukin (IL)-33-induced allergen-independent murine model of asthma

Yuan Linjie1, Chen Shihao1, An Gao1, Huang Qiong1, Yi Dawei1, Li Yan1, Lyu Zhe1, Wang Jingjing2, Huang Kewu3, Wang Wei1, Sun Ying1   

  1. 1. Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China;
    2. Department of Laboratory Animal Sciences, Capital Medical University, Beijing 100069, China;
    3. Department of Respiratory and Critical Care Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing Institute of Respiratory Medicine, Beijing 100020, China
  • Received:2016-06-30 Online:2016-10-21 Published:2016-10-19
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81373177, 81471594),Science and Technology Project of the Beijing Municipal Education Commission (KM201410025006).

Abstract: Objective To explore effects of IL-33 on subsets of T cells and B cells, type 2 innate lymphoid cells (ILC2) and natural killer T (NKT) cells in lungs in IL-33-induced murine model of asthma.Methods Mice were randomly distributed into two groups including normal saline(NS, control group) and IL-33-challenged groups. Nasal challenges with recombinant mouse IL-33 or saline were daily performed from the day 1-6,followed by every 2 days for a further 12 days. Lung functions and histological staining of lung tissue sections were used to measure airways hyperresponsiveness and inflammation.Flow cytometry was employed to determine the changes of total and phenotypes of subsets of pulmonary T cells and B cells,NKT cells and ILC2 cells, compared with those of lung. Results Compared with the NS group intranasal challenge with IL-33 induced airways hyperresponsiveness, infiltrating inflammatory cells and goblet cell hyperplasia. IL-33-challenge also increased total pulmonary numbers of cells, total CD3+T cells and type 2 helper cells (CD3+CD8-IL-4+) which leading to decrease of Th1/Th2 ratio (P<0.01). In addition, nasal challenge with IL-33 increased total number of CD19+B cells and their subsets (B1a:CD19+CD23-CD5+CD11b+, B1b:CD19+CD23-CD5-CD11b+ and B2 B cells:CD19+CD23+B220+) as well as ILC2(lineage-ICOS+ST2+) (P<0.01), but not NKT cells (CD3+CD8-CD49b+) (P>0.05).Conclusion Local challenge with IL-33 may play role in the pathogenesis of asthma through acting directly and/or indirectly on T cells, B cells and ILC2 cells, breaking the balance of immune system and causing immune dysfunction.

Key words: interleukin-33, asthma, T lymphocytes, B lymphocytes, type 2 innate lymphoid cells

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