C-reactive protein enhances the respiratory burst of neutrophils-induced by antineutrophil cytoplasmic antibody

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 (50 μg/mL, incubating for 30 min) could not active neutrophils alone, after incubation with neutrophils for 10 min, CRP (50 μg/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.

► CRP could influence the ANCA-induced respiratory burst of neutrophils. ► CRP can enhance the respiratory burst of neutrophils induced by ANCA against myeloperoxidse. ► CRP can prime neutrophils and increase the expression of membrane proteinase 3 of neutrophils. ► Heat-treated CRP cannot enhance the levels of neutrophils respiratory burst induced by ANCA or increase the expression of membrane proteinase 3 of neutrophils.