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Imaging Features of Systemic Sclerosis-Associated Interstitial Lung Disease
Published on: June 16, 2020
ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease
Airi Nishimi1, Takeo Isozaki2, Shinichiro Nishimi1
1Division of Rheumatology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan.
Abstract:
The "A disintegrin and metalloprotease" (ADAM) family is thought to play an important role in tissue destruction and inflammatory reactions. ADAM-17 was first described as the protease responsible for tumor necrosis factor (TNF)-α shedding. Here, we have shown the expression of ADAM-17 in inflammatory myopathy and demonstrated the role of inflammation in interstitial lung diseases (ILD). ADAM-17 in inflammatory myopathy serum [polymyositis (n = 26), dermatomyositis (n = 34), and clinically amyopathic dermatomyositis (n = 10)] and healthy control (n = 19) was measured using enzyme-linked immunosorbent assay. The relationship between ADAM-17 and clinical data was examined. Finally, we performed immunohistological analysis to investigate the expression of ADAM-17 on the muscles of the inflammatory myopathy patients. ADAM-17 in inflammatory myopathy was significantly higher than that in healthy control (mean ± SEM, 1048 ± 312 and 36 ± 18 pg/ml, respectively; p < 0.05). ADAM-17 in post-treatment with corticosteroid and/or immunosuppressant serum was significantly decreased compared with that in pre-treatment serum (1465 ± 562 and 1059 ± 503 pg/ml, respectively; p < 0.01). ADAM-17 was significantly positively correlated with fractalkine/CX3CL1 and CXCL16. In addition, ADAM-17 in inflammatory myopathy with ILD patients (n = 46) was significantly higher than that in non-ILD patients (n = 24) (1379 ± 454 and 413 ± 226 pg/ml, respectively; p < 0.05). We found the expression of ADAM-17 on muscle biopsy tissue. ADAM-17 is expressed in inflammatory myopathies especially ILD, suggesting that ADAM-17 plays a role in lung fibrosis. ADAM-17 may be a potential target in inflammatory myopathies with ILD.
Insights
A disintegrin and metalloprotease-17 (ADAM-17) is elevated in inflammatory myopathy patients, particularly those with interstitial lung disease (ILD). ADAM-17 levels decrease with treatment, suggesting it
Area of Science:
- Biochemistry
- Immunology
- Pulmonology
Background:
- A disintegrin and metalloprotease (ADAM) family proteins are implicated in tissue degradation and inflammation.
- ADAM-17 is known for its role in shedding tumor necrosis factor-alpha (TNF-α).
- The involvement of ADAM-17 in inflammatory myopathies and its association with interstitial lung diseases (ILD) require further investigation.
Purpose of the Study:
- To investigate the expression levels of ADAM-17 in patients with inflammatory myopathies.
- To explore the correlation between ADAM-17 and the presence of ILD.
- To assess the impact of treatment on ADAM-17 levels and its expression in muscle tissue.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to measure serum ADAM-17 levels in patients with polymyositis, dermatomyositis, and clinically amyopathic dermatomyositis, compared to healthy controls.
- Immunohistological analysis was performed on muscle biopsy samples from inflammatory myopathy patients.
- Statistical analysis examined the relationship between ADAM-17 levels, clinical data, and the presence of ILD.
Main Results:
- Serum ADAM-17 levels were significantly higher in inflammatory myopathy patients compared to healthy controls.
- ADAM-17 levels were significantly elevated in inflammatory myopathy patients with ILD compared to those without ILD.
- ADAM-17 levels significantly decreased after treatment with corticosteroids and/or immunosuppressants and correlated positively with fractalkine/CX3CL1 and CXCL16.
Conclusions:
- ADAM-17 is expressed in inflammatory myopathies, particularly in cases associated with ILD.
- The findings suggest a role for ADAM-17 in the pathogenesis of lung fibrosis in ILD.
- ADAM-17 may represent a potential therapeutic target for inflammatory myopathies with ILD.
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