Yanwu You1, Yueqiu Qin2, Xu Lin3, Fafen Yang4, Junjie Wang5, Fang Yuan6, Suren R Sooranna7, Liao Pinhu8. 1. Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. Electronic address: youyanwu@163.com. 2. Department of Gastroenterology, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. Electronic address: yyfyqyq@163.com. 3. Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. Electronic address: linyyfyy@163.com. 4. Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. Electronic address: wotanlong@163.com. 5. Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. Electronic address: 316200304@qq.com. 6. Department of Nephrology, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. Electronic address: yuanfang_1018@126.com. 7. Department of Surgery and Cancer, Imperial College London, Chelsea and Westminster Hospital, 369, Fulham Road, London SW10 9NH, UK. Electronic address: s.sooranna@imperial.ac.uk. 8. Department of Intensive Care Medicine, Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. Electronic address: liaopinhu@163.com.
Abstract
OBJECTIVE: To investigate the expression levels of fractalkine (FKN) mRNA in peripheral blood mononuclear cells (PBMCs) and FKN protein in serum of patients with lupus nephritis (LN) from China, and to evaluate the associations between the expression of FKN and systemic lupus erythematosus disease activity index 2000 (SLEDAI-2 K), anti-double-stranded DNA and complement proteins in LN patients. METHODS: Real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expression levels of FKN mRNA in PBMCs and FKN protein in serum separately from 105 patients with LN and 52 healthy controls. RESULTS: Serum level and mRNA level of FKN were significantly increased in LN patients when compared to controls (P < 0.001). Higher FKN levels were found in active LN patients and LN patients with renal damage when compared with inactive LN patients and LN patients without renal damage (P < 0.001). Higher serum FKN levels were detected in inactive LN patients in comparison with healthy controls (Z = -7.165, P < 0.001). The FKN expression levels were positively correlated with SLEDAI-2 K, and was associated with the presence of autoantibodies and negatively correlated with complement proteins C3 and C4 in LN patients. CONCLUSIONS: The results suggest that upregulation of FKN is associated with the pathogenesis and activity of LN in Chinese patients.
OBJECTIVE: To investigate the expression levels of fractalkine (FKN) mRNA in peripheral blood mononuclear cells (PBMCs) and FKN protein in serum of patients with lupus nephritis (LN) from China, and to evaluate the associations between the expression of FKN and systemic lupus erythematosus disease activity index 2000 (SLEDAI-2 K), anti-double-stranded DNA and complement proteins in LN patients. METHODS: Real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expression levels of FKN mRNA in PBMCs and FKN protein in serum separately from 105 patients with LN and 52 healthy controls. RESULTS: Serum level and mRNA level of FKN were significantly increased in LN patients when compared to controls (P < 0.001). Higher FKN levels were found in active LN patients and LN patients with renal damage when compared with inactive LN patients and LN patients without renal damage (P < 0.001). Higher serum FKN levels were detected in inactive LN patients in comparison with healthy controls (Z = -7.165, P < 0.001). The FKN expression levels were positively correlated with SLEDAI-2 K, and was associated with the presence of autoantibodies and negatively correlated with complement proteins C3 and C4 in LN patients. CONCLUSIONS: The results suggest that upregulation of FKN is associated with the pathogenesis and activity of LN in Chinese patients.