Home  About Journal Instructions for Authors Editorial Board Subscribe Advertisement Messages Board Contact Us 中文

CJAP ›› 2021, Vol. 37 ›› Issue (4): 423-428.doi: 10.12047/j.cjap.6126.2021.050

• ORIGINAL ARTICLES • Previous Articles     Next Articles

Progranulin attenuated asthma inflammation by inhibiting the expression of IL-6

QI Yu-hong1, SUN Si2, WANG Ling1, YANG Jing1, WU Guang-ying1, HUANG Qi1, XU Wen-chun1△   

  1. 1. Key Laboratory of Clinical Laboratory Diagnostics of Ministry of Education, Faculty of Laboratory Medicine, Chongqing Medical University, Chongqing 400016;
    2. The First People's Hospital Clinical Laboratory Of Chongqing Liang Jiang New Area, Chongqing 401147, China
  • Online:2021-07-28 Published:2021-08-09

Abstract: Objective: To investigate the role and mechanism of progranulin (PGRN) in asthma. Methods: Control group and model group were set up in wild and IL-6 knockout (IL-6 ko) mice, respectively. For asthma model, mice were intraperitoneally sensitized with 100 μg OVA on days 0 and 7, followed by aerosol challenges with 5% OVA for 30 min per day from day 14 to 21, and mice were sacrificed 24 h after the last challenge. The mice in control group were treated in the same way with PBS. Bronchoalveolar lavage fluid (BALF) was collected for leukocytes count and differential count. The pathological changes of lung tissues were observed by H&E staining. The cytokines in lung homogenate, serum and BALF were detected by Q-PCR and ELISA. The in vitro model of asthma was induced by stimulating A549 or BEAS-2B cells with IL-13. Each group was replicated in three wells and four groups were designed: PBS group, IL-13 treatment group, IL-13 + rhPGRN treatment group, inhibitors of p38 phosphorylation (SB203508) treatment group. The cells or supernatant were collected after 0~48 h. PGRN and IL-6 levels were determined by Q-PCR and ELISA, the level of p38 phosphorylation was tested by Western blot (WB). Results: Compared with control group, PGRN levels were decreased in lung homogenate and BALF (P<0.05), and PGRN presented a downtrend in serum, however, the level of IL-6 in BALF was increased in asthma mice (P<0.01). In IL-6 ko asthma mice, compared with the wild asthma mice, leukocytes, especially neutrophils in BALF were decreased (P<0.05), but PGRN was increased (P<0.05), lung pathological damage was significantly alleviated. In vitro experiments, compared with PBS group, PGRN level was decreased (P<0.05), IL-6 level was increased (P<0.01), phosphorylation of p38 was activated in IL-13 treatment group. Compared with IL-13 treatment group, in IL-13 + PGRN treatment group, IL-6 level was decreased (P<0.05); phosphorylation of p38 was inhibited (P<0.05); and the production of IL-6 (P<0.05) was decreased after treatment with inhibitor of p38 phosphorylation. Conclusion: PGRN inhibited the production of IL-6 by suppressing the p38 phosphorylation to alleviate asthmatic airway inflammation.

Key words: mice, asthma, airway inflammation, PGRN, interleukin-6

CLC Number: 

Copyright © 2015 CJAP, All Rights Reserved.
Powered by Beijing Magtech Co. Ltd