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-alpha 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 mu g/mL, incubating for 30 min) could not active neutrophils alone, after incubation with neutrophils for 10 min, CRP (50 mu g/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. (C) 2012 Elsevier Ltd. All rights reserved.http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000307489800007&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=8e1609b174ce4e31116a60747a720701Biochemistry & Molecular BiologyImmunologySCI(E)PubMed1ARTICLE3-4148-1545