C-reactive protein enhances the respiratory burst of neutrophils-induced by antineutrophil cytoplasmic antibody.
C-reactive protein enhances the respiratory burst of neutrophils-induced by antineutrophil cytoplasmic antibody.
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DOI:
10.1016/j.molimm.2012.05.012
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发表时间:
2012-10
影响因子:
3.6
通讯作者:
Peng-Cheng Xu;J. Hao;Xiao-wei Yang;D. Chang;Min Chen;Ming-Hui Zhao
中科院分区:
文献类型:
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作者:
Peng-Cheng Xu;J. Hao;Xiao-wei Yang;D. Chang;Min Chen;Ming-Hui Zhao
Serum C-reactive protein (CRP) was one of the useful biomarkers for evaluating the disease activity in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). Cumulating studies proved that CRP was pathogenic in a variety of diseases. In the current study, the in vitro effects of CRP to prime neutrophils for ANCA-induced respiratory burst were investigated with flow cytometry. Without TNF-α in the reactive system, ANCA could only induce a slight level of respiratory burst of neutrophils. CRP could enhance the respiratory burst of neutrophils induced by ANCA against myeloperoxidse [mean fluorescence intensity (MFI, 68.45±16.87 vs. 58.65±15.09, P<0.05) or by ANCA against proteinase 3 (MFI, 79.51±15.90 vs. 61.73±14.89, P<0.05). Although CRP (50μg/mL, incubating for 30min) could not active neutrophils alone, after incubation with neutrophils for 10min, CRP (50μg/mL) could increase the expression of membrane proteinase 3 of neutrophils (MFI, 365.27±143.50 vs. 235.32±124.65, P<0.05). Heat-treated CRP could not enhance the levels of neutrophils respiratory burst induced by ANCA or increase the expression of membrane proteinase 3 of neutrophils. So CRP can prime neutrophils and enhance the respiratory burst induced by ANCA and might be pathogenic in AAV.