Allergy and Airway: Asthma III |

Dynamic Analysis of Accumulation of Type 2 Innate Lymphoid Cells in Tissues and Organs in IL-25 and IL-33-Induced Murine Models of Asthma FREE TO VIEW

Yan Li; Zhe Lv; Jingjing Wang; Yafei Chi; Ping Huang; Chris Corrigan; Kewu Huang; Wei Wang; Sun Ying
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Capital Medical University, Beijing, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A27. doi:10.1016/j.chest.2016.02.029
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SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Type 2 innate lymphoid cells (ILC2) play important role in the pathogenesis of asthma because of producing large amounts of Th2-type cytokines. The mechanisms of ILC2 chemotaxis into lungs, however, are still unclear. We aimed to compare dynamic accumulation of ILC2 into various organs and tissues in IL-25- and IL-33-induced murine models of asthma and to explore the potential mechanisms of ILC2 chemotaxis.

METHODS: BALB/c mice were intranasally changed with murine IL-25 or IL-33, while OVA and saline challenged mice were used as positive and negative controls. Bone marrow, spleen, thymus, mesenteric lymph nodes, mediastinal lymph nodes, lung tissue and bronchoalveolar lavage fluid (BALF) were collected from the mice at experimental acute, subacute, chronic and convalescent phases. Flow cytometry, in vitro chemotaxis assay and small animal in vivo imaging were used to measure the distribution and abundance and chemotaxis of ILC2 in vitro and in vivo.

RESULTS: Compared with the control group, both IL-25 and IL-33 alone induced accumulation of ILC2 into mediastinal lymph nodes, lung tissue and BALF, but with different kinetics. When gathering its phases, the peak of IL-25 induced ILC2 accumulation into lung tissue and BALF was earlier than that of the IL-33-induced mice. In quantity, the numbers of ILC2 in BALF, lung tissue and mediastinal lymph nodes were significantly higher in IL-33-induced mice compared with IL-25-induced mice. In vitro IL-33 directly induced ILC2 chemotaxis while IL-25 did not. The results of small animal in vivo imaging technology further confirmed that single intranasally inhalation of IL-33 was sufficient to induce accumulation of injected ILC2 through tail vein into the lungs.

CONCLUSIONS: The data suggest that airways epithelium-derived IL-25 or IL-33 can induce accumulation of ILC2 to the lungs and that IL-33 has direct effect on ILC2 chemotaxis.

CLINICAL IMPLICATIONS: Our data suggest that ILC2 may be involved in the pathogenesis of asthma, and that targeting IL-33 may therefore be a new target for asthma intervention strategies.

DISCLOSURE: The following authors have nothing to disclose: Yan Li, Zhe Lv, Jingjing Wang, Yafei Chi, Ping Huang, Chris Corrigan, Kewu Huang, Wei Wang, Sun Ying

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