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ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease

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A Correction to this article was published on 10 March 2018

This article has been updated

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.

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Change history

  • 10 March 2018

    The original version of this article, unfortunately, contained errors. Figure citation, caption, image and updated sentence in the Result section are now presented correctly in this article.

Abbreviations

ILD:

interstitial lung disease

ADAM:

A disintegrin and metalloprotease

TNF:

tumor necrosis factor

PM:

polymyositis

DM:

dermatomyositis

CADM:

clinically amyopathic dermatomyositis

ADM:

amyopathic DM

EAM:

experimental autoimmune myositis

HDM:

hypomyopathic dermatomyositis

CK:

creatine kinase

ELISA:

enzyme-linked immunosorbent assay

LDH:

lactate dehydrogenase

FBS:

fetal bovine serum

PBS:

phosphate buffered saline

HLF:

human lung fibroblasts

IL-6R:

interleukine-6 receptor

RA:

rheumatoid arthritis

ST:

synovial tissue

OA:

osteoarthritis

TACE:

tumor-necrosis-factor-converting-enzyme

AREG:

amphiregulin

TGF:

transforming growth factor

MHC-I:

major histocompatibility complex I

IP-10/CXCL10:

interferon gamma-induced protein-10/CXCL10

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Acknowledgements

We thank Ms. Takeuchi for performing all ELISAs.

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Authors and Affiliations

  1. Division of Rheumatology, Department of Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8666, Japan

    Airi Nishimi, Takeo Isozaki, Shinichiro Nishimi, Sho Ishii, Takahiro Tokunaga, Hidekazu Furuya, Kuninobu Wakabayashi & Tsuyoshi Kasama

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  1. Airi Nishimi
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  2. Takeo Isozaki
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  3. Shinichiro Nishimi
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  4. Sho Ishii
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Contributions

AN performed all assays with assistance from TI, SN, SI, TT, HF, and KW. TI also assisted with the acquisition of data. AN performed the statistical analysis. TI, KW, and TK conceived the study and participated in its design and coordination. TI assisted AN with drafting the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Takeo Isozaki.

Ethics declarations

We obtained written informed consent from all patients who enrolled in the study. The study received approval from the Bio-Ethics Committee of the Department of Medicine, Showa University School of Medicine (No. 1892).

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Nishimi, A., Isozaki, T., Nishimi, S. et al. ADAM-17 is expressed in the inflammatory myopathy and is involved with interstitial lung disease. Clin Rheumatol 37, 1017–1024 (2018). https://doi.org/10.1007/s10067-018-4014-5

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  • DOI: https://doi.org/10.1007/s10067-018-4014-5

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