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1.
Chinese Journal of Immunology ; (12): 151-155, 2019.
Article in Chinese | WPRIM | ID: wpr-744624

ABSTRACT

Objective: To investigate the expression of IL-38 and MIP-2 in lung tissue of rats with pulmonary fibrosis induced by bleomycin, and to explore the significance of IL-38 and MIP-2 in pulmonary fibrosis in rats. Methods: 45 Wistar rats were randomly divided into saline control group ( group N), bleomycin group ( group B) and dexamethasone group ( group D) according to the random and control principle. On the 7 th, 14 th, and 28 th day, 5 rats were killed in each group. The pathological changes of lung tissue were observed by hematoxylin-eosin ( HE) staining in lung tissue. The expression of IL-38 and HYP in lung tissue of rats was measured by enzyme linked immunoassay ( ELISA) and the expression of MIP-2 in lung tissue of rats was measured by RT-PCR method. Results: (1) HE staining showed that the lung tissue from group B and group D developed from normal to inflammatory changes to pulmonary fibrosis. (2) The expression of IL-38 in group B and D decreased gradually, and the decrease was most obvious at 28 th day, which was lower than that in group N ( P<0. 05), and the expression of IL-38 in group B was lower than that in D group, and the difference was statistically significant ( P<0. 05). (3) The expression of MIP-2 and HYP increased gradually in group B and D, which were higher than those in group N, and the difference was statistically significant ( P<0. 05). The MIP-2 and HYP expressions in group B were higher than those of group D in the same period, and the difference was statistically significant ( P<0. 05). Conclusion: IL-38 and MIP-2 play an important role in the occurrence and development of bleomycin induced pulmonary fibrosis in rats. The application of dexamethasone can improve the degree of pulmonary fibrosis in rats. The effect may be related to the up-regulation of IL-38 and the downregulation of MIP-2.

2.
Chinese Journal of Immunology ; (12): 251-255, 2018.
Article in Chinese | WPRIM | ID: wpr-702711

ABSTRACT

Objective:To investigate the role and mechanism of IL-38 in inhibiting osteoporosis.Methods:A total of 138 cases of patients with osteoporosis in our hospital from June 2014 to December 2016 were recruited.Another 120 cases of fracture surgery patients without osteoporosis were selected as control.Serum levels of IL-38 in different groups were determined using a commercially available sandwich ELISA (Enzyme-Linked ImmunoSorbent Assay).Construction of IL-38-C57BL/6J transgenic mice,the wild type and IL-38 transgenic mice were set to sham operation group (Sham),operation group (ovariectomy,group OVX) respectively.After 8 weeks of the operation,the serum level of alkaline phosphatase(ALP),calcium and phosphorus were detected.The bilateral femur and spine of mice were collected after sacrifice,the morphology and structure of the femur were analyzed,and the bone density was measured by bone density meter.The bone marrow stromal cells(BMSCs) were isolated and the invitro proliferation ability of BMSCs were meas-ured.Western blot were used to detect the phosphorylation level of PI3K,Akt,GSK3β and NFATc1 in BMSCs.After transfection of IL-38 into mouse osteoblast MC3T3-E1 cell,the phosphorylation level of PI3K,Akt,GSK3β and NFATc1 were detected by Western blot.Apoptosis of MC3T3-E1 cells were detected by flow cytometry.Results:The serum level of IL-38 in patients with osteoporosis were significant lower than control group(P<0.05).The serum level of estrogen,calcium and phosphorus in OVX group of wild type and IL-38 transgenic mice were significant lower than the sham operation group(P<0.05),while the level of ALP was significant higher than sham operation group (P<0.05),but the serum level of calcium and phosphorus in OVX group of IL-38 transgenic mice were significant higher than wild type mice(P<0.05).The pathological section of femur and spine BMD showed that the bone tissue in wild type mice and IL-38 transgenic mice in OVX group were damaged and the bone density decreased significantly,but IL-38 transgenic mice was significant better than wild type mice (P<0.05).The proliferation ability of BMSCs in OVX group of IL-38 transgenic mice was significant higher than wild type mice (P<0.05).The phosphorylation level of PI3K,Akt and NFATc1 in OVX group of IL-38 transgenic mice were significant lower than wild type mice(P<0.05),while the phosphorylation level of GSK3β was significant higher than wild type mice (P<0.05).After transfection of IL-38 into MC3T3-E1 cell,the phosphorylation level of PI3K,Akt and NFATc1 were significant decreased (P<0.05),while the phosphorylation level of GSK3β was significant increased (P<0.05).Flow cytometry assay showed that IL-38 transfection significant decreased the apoptosis of MC3T3-E1 cells(P<0.05).Conclusion:The serum level of IL-38 in patients with osteoporosis is decreased significantly.IL-38 may inhibit the proliferation of BMSCs and inhibit the apoptosis of osteoblasts by regulating the PI3K/Akt/GSK3β/NFATc1 signaling pathway.

3.
Chinese Journal of Immunology ; (12): 1647-1651, 2017.
Article in Chinese | WPRIM | ID: wpr-667791

ABSTRACT

Objective:To investigate the proteins association of IL-38 and TLR4 in rheumatoid arthritis (RA) and its mechanism in RA pathogenesis.Methods:Forty-one rheumatoid arthritis patients(observation group) and forty-five patients with post-traumatic synovial membrane resection (control group) in our hospital from Jan 2013 to Feb 2016 were selected as study subjects.Peripheral blood mononuclear cells (PBMCs),synovial tissues and serum from patients with RA and controls were collected.The expression of IL-38 and TLR4 in PBMCs and synovial tissues were detected by real-time polymerase chain reaction (realtime-PCR).The protiens of IL-38 and TLR4 in synovial tissues and fluid from RA patients and controls were detected by enzyme-linked immunosorbent assay (ELISA) or Western blot assay,respectively.RAW264.7 cells were stimulated by lipopolysaccharide (LPS) and/or IL-38.The production of inflammatory cytokines including IL-6,IL-8 as well as TNF-α were detected by real-time-PCR and ELISA,respectively.The activation of nuclear factor-κB(NF-κB) signaling were determined by nuclear transfer reagent kit for NF-κB and Western blot.Results: Compared with control group,the expression of IL-38 in PBMCs,synovial tissue,serum and synovial fluid of patients with RA increased significantly,meanwhile,TLR4 was significantly increased in PBMCs and synovium of RA patients.Moreover,IL-38 was negatively associated with TLR4 in RA,suggested by Pearson′s correlation analysis.When RAW264.7 cells were stimulated by LPS with or without IL-38 in vitro,IL-38 could suppress LPS-mediated expression of TLR4 and the production of IL-6,IL-8 and TNF-α in RAW264.7 cells.IL-38 can inhibit the activation of NF-κB signaling pathway,so we hypothesized that IL-38 may inhibit the expression of inflammatory factor which induced by LPS/TLR4 signaling via inhibiting the activation of NF-κB signaling pathway.Conclusion: IL-38 can attenuates rheumatoid arthritis through inhibiting LPS/TLR4 induced inflammation in rheumatoid arthritis,and the mechanism may be through inhibiting the activation of NF-κB signaling pathway.

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