Research Paper Volume 13, Issue 17 pp 21729—21742
Cytokine antibody array-based analysis of IL-37 treatment effects in asthma
- 1 Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences/Peking Union Medical College, Beijing 100730, China
- 2 Department of Respiratory and Critical Care Medicine, China-Japan Friendship Hospital, Beijing 10029, China
- 3 Institute of Clinical Medicine Science, China-Japan Friendship Hospital, Beijing 10029, China
- 4 Peking University China-Japan Friendship School of Clinical Medicine, Beijing 10029, China
Received: April 26, 2021 Accepted: July 8, 2021 Published: September 13, 2021https://doi.org/10.18632/aging.203515
How to Cite
Copyright: © 2021 Gao et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Asthma is driven by group 2 innate lymphoid cells, antigen-specific CD4+ T helper type 2 cells and their cytokines such as interleukin (IL)-4, IL-5, IL-13. IL-37 is decreased in asthma and negatively related to Th2 cytokines and other pro-inflammatory cytokines. Our study showed that IL-37 level in asthmatic peripheral blood mononuclear cells was lower than in healthy. Further, IL-37 was negatively correlated with exhaled nitric oxide, asthma control test score, atopy and rhinitis history in asthmatics. Then an OVA-induced asthma mice model treated with rhIL-37 was established. An antibody array was employed to uncover altered cytokines induced by IL-37 in mice lung tissue. 20 proteins differentially expressed after rhIL-37 treatment and five of them were validated in asthmatic peripheral blood mononuclear cells. Consistent with cytokine antibody array, CCL3, CCL4, CCL5 decreased after IL-37 administration. While CXCL9 and CXCL13 were no change. We concluded that IL-37 reduce asthmatic symptoms by inhibit pro-inflammatory cytokine such as CCL3, CCL4, CCL5.