Y-J Zhang1, Q Zhang1, G-J Yang2, J-H Tao2, G-C Wu1, X-L Huang1, Y Duan1, X-P Li2, D-Q Ye3, J Wang4. 1. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Meishan Road 81, 230032, Hefei, Anhui, China. 2. Department of Rheumatology and Immunology, Anhui Medical University, Anhui Provincial Hospital, Hefei, China. 3. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Meishan Road 81, 230032, Hefei, Anhui, China. ydq@ahmu.edu.cn. 4. Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Meishan Road 81, 230032, Hefei, Anhui, China. jwang2006@126.com.
Abstract
PURPOSE OF THE STUDY: Systemic sclerosis (SSc) is a multisystem autoimmune disease. Although the pathogenesis of the disease remains incompletely understood, some cytokines or growth factors which regulate SSc induction may be involved in the injury of endothelial cells and the modulation of leukocyte function. We aimed to perform this case-control study to determine serum levels of interleukin (IL)-1α, IL-1β, IL-18 and IL-33 and their associations with clinical manifestations in SSc patients. MATERIALS AND METHODS: There were 56 patients with SSc and 56 healthy individuals who were recruited from local hospital between 2012 and 2014. Serum IL-1α, IL-1β, IL-18 and IL-33 levels were measured with specific enzyme-linked immunosorbent assay kits. RESULTS: Univariate analysis revealed that serum IL-1β, IL-18 and IL-33 levels in SSc patients were significantly higher than that in healthy controls. After adjusting possible confounding factors (sex, age, smoking and drinking) by multivariable analyses, serum IL-1β levels (OR = 1.082; 95 % CI: 1.013-1.155) and serum IL-33 levels (OR = 1.100; 95 %CI: 1.022-1.185) were still related factors. There were interrelationships among the serum levels of IL-1α, IL-1β, IL-18 and IL-33 and these associations were not consistent in SSc patients and controls. No associations of serum IL-1α, IL-1β, IL-18 and IL-33 levels with clinical parameters were found. CONCLUSION: IL-1β and IL-33 may contribute to the development of SSc. While there were no direct associations between these cytokines and disease manifestations, they still could be considered as serum markers of development of SSc. Further studies are required to validate this incipient data.
PURPOSE OF THE STUDY: Systemic sclerosis (SSc) is a multisystem autoimmune disease. Although the pathogenesis of the disease remains incompletely understood, some cytokines or growth factors which regulate SSc induction may be involved in the injury of endothelial cells and the modulation of leukocyte function. We aimed to perform this case-control study to determine serum levels of interleukin (IL)-1α, IL-1β, IL-18 and IL-33 and their associations with clinical manifestations in SSc patients. MATERIALS AND METHODS: There were 56 patients with SSc and 56 healthy individuals who were recruited from local hospital between 2012 and 2014. Serum IL-1α, IL-1β, IL-18 and IL-33 levels were measured with specific enzyme-linked immunosorbent assay kits. RESULTS: Univariate analysis revealed that serum IL-1β, IL-18 and IL-33 levels in SSc patients were significantly higher than that in healthy controls. After adjusting possible confounding factors (sex, age, smoking and drinking) by multivariable analyses, serum IL-1β levels (OR = 1.082; 95 % CI: 1.013-1.155) and serum IL-33 levels (OR = 1.100; 95 %CI: 1.022-1.185) were still related factors. There were interrelationships among the serum levels of IL-1α, IL-1β, IL-18 and IL-33 and these associations were not consistent in SSc patients and controls. No associations of serum IL-1α, IL-1β, IL-18 and IL-33 levels with clinical parameters were found. CONCLUSION: IL-1β and IL-33 may contribute to the development of SSc. While there were no direct associations between these cytokines and disease manifestations, they still could be considered as serum markers of development of SSc. Further studies are required to validate this incipient data.
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