Serum periostin levels: A potential serologic marker for toluene diisocyanate-induced occupational asthma

Ji Ho Lee, Sang Ha Kim, Youngwoo Choi, Hoang Kim Tu Trinh, Eun Mi Yang, Ga Young Ban, Yoo Seob Shin, Young Min Ye, Kenji Izuhara, Hae Sim Park

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)

Abstract

Purpose: Toluene diisocyanate (TDI) is a leading cause of occupational asthma (OA). Periostin is a matricellular protein implicated in type 2 immunity-driven asthma. Its pathogenic role in TDI-OA has not been completely elucidated. The present study was performed to investigate the role of periostin in TDI-OA. Materials and Methods: Serum periostin levels were measured in subjects with TDI-OA, asymptomatic TDI-exposure controls (AECs), non-occupational asthmatics (NAs), and unexposed normal controls (NCs). To understand the mechanism by which TDI induces periostin production, primary small airway epithelial cells (SAECs) were cultured under stimulation of TDI and neutrophils from asthmatic patients. Results: Fifty-three subjects with TDI-OA, 71 AECs, 67 NAs, and 83 NCs were enrolled. Serum periostin levels were significantly higher in TDI-OA subjects than in AECs (p=0.001), NAs (p<0.001), and NCs (p<0.001). In TDI-exposed subjects (TDI-OA and AEC), the PC 20 methacholine levels were significantly lower in subjects with a higher periostin level than in those with a lower periostin level. TDI exposure did not increase periostin production directly by SAECs; however, periostin production increased significantly after co-culture with TDI and neutrophils, which was suppressed by an antioxidant. In addition, increased release of TGF-β1 was noted from SAECs when exposed to TDI and neutrophils, which was also suppressed by an antioxidant. Conclusion: These results suggest that an increased periostin level may contribute to the progression of airway inflammation to remodeling in TDI-exposed workers. A high serum periostin level is a potential serologic marker of the phenotype of TDI-OA.

Original languageEnglish
Pages (from-to)1214-1221
Number of pages8
JournalYonsei medical journal
Volume59
Issue number10
DOIs
Publication statusPublished - 2018 Dec

Bibliographical note

Funding Information:
This research was supported by a grant (HI14C2628) from the Korea Health Technology R&D Project through the Korea Health Industry Development Institute, funded by the Ministry of Health & Welfare, Republic of Korea and a grant from the Korean Society of Occupational Asthma and Lung Diseases.

Publisher Copyright:
© Yonsei University College of Medicine 2018.

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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