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Increased macrophage migration inhibitory factor is associated with inflammation in patients with rheumatoid
Haolin Wu1, Fanzhang Yin1, Yue Wang1
1Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, China.
Objective:
The macrophage migration inhibitory factor (MIF) in the plasma, hydrops articuli, and synovium, and its relationship with laboratory indexes in patients with rheumatoid arthritis (RA) were determined, for the purpose to reveal the role of MIF on the pathogenesis of RA.
Methods:
MIF mRNA expression in PBMCs was detected by qPCR. Plasma MIF was measured by enzyme linked immunosorbent assay (ELISA). MIF in hydrops articuli and synovium from RA patients and OA patients was evaluated by immunofluorescence (IF) and immunohistochemistry (IHC). The relationship between MIF and laboratory indexes of RA patients was analyzed. Human fibroblast-like synoviocytes (FLS) were treated with recombinant human MIF, and expression of inflammatory factors was determined by qPCR. The matrix metalloproteinase (MMP) 9 and extracellular regulated protein kinases (ERK)1/2 in FLS with MIF treatment were detected.
Results:
MIF is significantly increased in plasma and hydrops articuli in RA patients. The expression of multiple inflammatory factors and MMPs was increased in RA patients and in FLS with rhMIF treatment. MIF was correlated with laboratory indexes in RA patients. Mechanistically, MIF promoted production of MMP9 by FLS through the ERK1/2 pathway.
Conclusion:
Our results indicated that increased MIF was correlated with disease activity of RA patients. These findings also suggested that MIF induced multiple inflammatory factors and MMP 9 in FLS via ERK 1/2 pathway. Key Points • MIF plays a key role in the initiation of RA by promoting the expression of various inflammatory factors in FLS and MMPs. • This study provides a basis for MIF-targeted RA clinical therapy and for exploring the feasibility of MIF as a therapeutic target for RA. • Increased MIF correlates with disease activity in RA patients.
Insights
Macrophage migration inhibitory factor (MIF) is elevated in rheumatoid arthritis (RA) and drives disease by increasing inflammatory factors and MMPs via the ERK1/2 pathway, suggesting MIF as a therapeutic target.
Area of Science:
- Rheumatology
- Immunology
- Molecular Biology
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation.
- The role of macrophage migration inhibitory factor (MIF) in RA pathogenesis requires further elucidation.
Purpose of the Study:
- To determine MIF levels in RA patients and its relationship with disease activity.
- To investigate the role of MIF in the pathogenesis of RA, particularly in fibroblast-like synoviocytes (FLS).
Main Methods:
- Quantification of MIF in plasma, synovial fluid, and tissue using ELISA, qPCR, immunofluorescence, and immunohistochemistry.
- Analysis of MIF correlation with laboratory markers of RA disease activity.
- In vitro studies involving recombinant human MIF treatment of FLS to assess inflammatory factor and MMP expression via the ERK1/2 pathway.
Main Results:
- MIF levels are significantly increased in the plasma and synovial fluid of RA patients.
- MIF treatment of FLS leads to increased expression of inflammatory factors and matrix metalloproteinase 9 (MMP-9).
- MIF promotes MMP-9 production in FLS through the extracellular regulated protein kinases (ERK)1/2 pathway and correlates with RA disease activity.
Conclusions:
- Elevated MIF is associated with disease activity in RA patients.
- MIF contributes to RA pathogenesis by inducing inflammatory factors and MMP-9 in FLS via the ERK1/2 pathway.
- MIF represents a potential therapeutic target for RA clinical therapy.
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