Journal
JOURNAL OF RHEUMATOLOGY
Volume 46, Issue 12, Pages 1560-1569Publisher
J RHEUMATOL PUBL CO
DOI: 10.3899/jrheum.181058
Keywords
ADULT-ONSET STILL DISEASE; NEUTROPHIL; PATHOGENESIS; NEUTROPHIL EXTRACELLULAR TRAP; DISEASE ACTIVITY
Categories
Funding
- Basic Science Research Program through the National Research Foundation of Korea - Ministry of Education, Science and Technology [2016R1C1B1014838]
- National Research Foundation of Korea [2016R1C1B1014838] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Ask authors/readers for more resources
Objective. Release of neutrophil extracellular traps (NET) has been described as an effector mechanism of polymorphonuclear neutrophils in several inflammatory diseases. Thus, this study was performed to evaluate the role of NET in the pathogenesis of adult-onset Still disease (AOSD). Methods. We determined the serum levels of NET molecules and investigated their associations with clinical disease activities in patients with AOSD. Further, we analyzed the differences in the NETosis response in AOSD patients compared to healthy controls (HC). To explore the in vivo involvement of NET in AOSD, we performed immunohistochemical analysis of skin and lymph node (LN) biopsies for proteins related to NET in patients with active AOSD. Results. Serum levels of cell-free DNA, myeloperoxidase (MPO)-DNA complex, and alpha-defensin were significantly increased in patients with AOSD compared to HC. Serum levels of the NET molecules, cell-free DNA, MPO-DNA, and alpha-defensin were correlated with several disease activity markers for AOSD. In followup of patients with AOSD after treatment with corticosteroid, the levels of cell-free DNA and alpha-defensin decreased significantly. On immunohistochemistry, neutrophil elastase-positive and MPO-positive inflammatory cells were detected in skin and LN of patients with AOSD, and were expressed in fiber form in the lesions. The serum from patients with active AOSD induced NETosis in neutrophils from HC. NET molecules induced interleukin 1 beta production in monocytes, representing a novel mechanism in the pathogenesis of AOSD. Conclusion. The findings presented here suggest that NET may contribute to the inflammatory response and pathogenesis in AOSD.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available