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Serum levels of interleukin‐18‐binding protein isoform a: Clinical association with inflammation and pulmonary hypertension in systemic sclerosis
Author(s) -
Nakamura Kouki,
Asano Yoshihide,
Taniguchi Takashi,
Minatsuki Shun,
Inaba Toshiro,
Maki Hisataka,
Hatano Masaru,
Yamashita Takashi,
Saigusa Ryosuke,
Ichimura Yohei,
Takahashi Takehiro,
Toyama Tetsuo,
Yoshizaki Ayumi,
Miyagaki Tomomitsu,
Sugaya Makoto,
Sato Shinichi
Publication year - 2016
Publication title -
the journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.9
H-Index - 65
eISSN - 1346-8138
pISSN - 0385-2407
DOI - 10.1111/1346-8138.13252
Subject(s) - systemic inflammation , pulmonary hypertension , inflammation , medicine , gene isoform , immunology , chemistry , biochemistry , gene
Systemic sclerosis ( SS c) is a chronic autoimmune inflammatory disease characterized by extensive tissue fibrosis and various vascular complications. A wealth of evidence suggests the substantial contribution of pro‐inflammatory cytokines to the development of SS c, but the role of interleukin ( IL )‐18 signaling in this disease still remains elusive. To address this issue, we herein determined serum levels of IL ‐18‐binding protein isoform a ( IL ‐18 BP a), a soluble decoy receptor for IL ‐18, by enzyme‐linked immunosorbent assay in 57 SS c patients and 20 healthy controls and evaluated their clinical correlation. Serum IL ‐18 BP a levels were higher in SS c patients than in healthy controls, while comparable between diffuse cutaneous SS c and limited cutaneous SS c patients. Although serum IL ‐18 BP a levels were not associated with dermal and pulmonary fibrotic parameters in SS c patients, there was a significant positive correlation between serum IL ‐18 BP a levels and right ventricular systolic pressure estimated by echocardiography. Furthermore, in 24 SS c patients who underwent right heart catheterization, serum IL ‐18 BP a levels positively correlated with mean pulmonary arterial pressure. As for systemic inflammatory markers, significant positive correlations of circulating IL ‐18 BP a levels with erythrocyte sedimentation rate and C‐reactive protein were noted. These results suggest that the inhibition of IL ‐18 signaling by IL ‐18 BP a may be involved in the development of pulmonary vascular involvement leading to pulmonary hypertension and modulate the systemic inflammation in SS c.