H-Index
75
Scimago Lab
powered by Scopus
JCR
Clarivate
Analytics
18%
Acceptance
Rate
call: +1.631.470.9640
Mon-Fri 10 am - 2 pm EST

Logo



eISSN: 1643-3750

Get your full text copy in PDF

Interleukin-37 (IL-37) Suppresses Pertussis Toxin-Induced Inflammatory Myopathy in a Rat Model

Peng Yan, Yuankai Zhang, Chunxiao Wang, Fang Lv, Lijun Song

(Department of Rheumatology, Qilu Hospital of Shandong University, Ji’nan, Shandong, China (mainland))

Med Sci Monit 2018; 24:9187-9195

DOI: 10.12659/MSM.910904


BACKGROUND: Recent data have demonstrated the potential immunosuppressive roles of interleukin-37 (IL-37) in several diseases, but whether it is involved in the pathogenesis of inflammatory myopathy has not been elucidated.
MATERIAL AND METHODS: An experimental autoimmune myositis (EAM) model was built by subcutaneous injections of pertussis toxin (PTX) and purified rabbit myosin (10mg/kg) emulsified with an equal volume of conventional complete Freund’s adjuvant (CFA) in a Lewis model. Autoimmune myositis Lewis model rats were divided into 3 groups: group A rats (control group) were injected with CFA in saline weekly; group B (IL-37 group) rats were injected with saline with IL-37 and CFA in saline weekly; and group C (IL-37 + SIS3 group) rats were injected with IL-37, CFA, and SIS3. ELISA was also used to assess the expressions of TNF-α, IL-6, IL-1β, TGF-β1, and CK. HE staining was performed to assess pathological changes in lung and muscle tissues.
RESULTS: The expressions of TNF-α, IL-6, IL-1β, TGF-β1, and CK significantly increased in autoimmune myositis Lewis model rats. After IL-37 treatment, the expression of TNF-α, IL-6, IL-1β, TGF-β1, and CK was significantly reduced, as were the inflammatory responses of lung and muscle. However, SIS3 reduced the effects of IL-37 on the autoimmune myositis Lewis model rats.
CONCLUSIONS: These findings indicate that IL-37 protects against inflammatory response via regulating Smad3 in autoimmune myositis Lewis model rats.

This paper has been published under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially.
I agree