Irisin Activates M1 Macrophage and Suppresses Th2-Type Immune Response in Rats with Pelvic Inflammatory Disease

OBJECTIVE: To investigate the mechanism of irisin to treat rats with acute pelvic inflammatory disease (APID). METHODS: Female rats were established as APID. Firstly, the content of IL-6, IL-8, TNF-α, and NF-kB was tested in rats' serum by enzyme linked immunosorbent assay (ELISA). Interferon-γ (IFN-γ) and IL-4 in the supernatant of pelvic homogenates were also detected. The mRNA expression of the inducible nitric oxide synthase (iNOS), TNF-α, chemokine ligand 1 (CXCL1), arginase-1(Arg1), and chitinase-3-like-3 (Chi313) genes in the pelvic cavity was detected by quantitative reverse transcription polymerase chain reaction (RT-qPCR). IFN-γ and IL-4 secreted by spleen CD4(+)T cells and CD8(+)T cells were counted by flow cytometry, and the ratio of IFN-γ/IL-4 in CD4(+)T cells and CD8(+)T cells in the spleen was also detected by flow cytometry. RESULTS: Irisin reduced the levels of IL-6, IL-8, TNF-α, and NF-kB in serum. Compared with the APID group, the expression level of IL-4 in the APID + Irisin group was reduced in the homogenate. At the same time, Irisin promotes the activation of M1 macrophages in the uterus, ovaries, and uterine tubes of rats with APID. Irisin also inhibited Th2-type immune response. CONCLUSIONS: Irisin activates M1 macrophage and suppresses Th2-type immune response in APID rats.