Abstract: Chen Jingsi, Sun Chen, Yang Haiping, Gan Liqiang, Tan Chunhua, Wang Hua, Luo Xiaoyan Department of Dermatology, Children′s Hospital of Chongqing Medical University （Chen JS, Gan LQ, Tan CH, Wang H, Luo XY）; Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics, Chongqing 400014, China （Sun C）; China International Science and Technology Cooperation Base of Child Development and Critical Disorders, Chongqing 400014, China （Yang HP） Corresponding author: Luo Xiaoyan, Email: luoxycq@hotmail.com 【Abstract】 Objective To investigate the role of neutrophils and their IgA Fc receptor CD89 in the occurrence of Henoch-Sch?nlein purpura （HSP）, to evaluate their effects on vascular endothelial cell apoptosis, and to explore their mechanisms. Methods Peripheral blood neutrophils were isolated from 30 children with acute HSP and 9 age-matched healthy controls separately. After isolation of serum IgA by Jacalin affinity chromatography, IgA was purified by polypropylene dextran gel chromatography. Real-time fluorescence-based quantitative PCR （qPCR） and Western blot analysis were performed to determine the mRNA and protein of CD89 on neutrophils respectively, and flow cytometry was conducted to measure the of neutrophil activation marker CD11b. Human umbilical vein endothelial cells （HUVEC） were co-cultured with neutrophils isolated from patients with HSP （HSP group） and healthy controls （healthy control group） separately. Moreover, the HSP group were divided into 3 subgroups to be treated with serum IgA isolated from the HSP patients （HSP IgA group）, monomeric IgA （mIgA group） and phosphate-buffered saline （blank control group） respectively. Then, flow cytometry was conducted to detect apoptosis of co-cultured HUVEC, and enzyme-linked immunosorbent assay（ELISA）to measure levels of interleukin-8 （IL-8） and tumor necrosis factor-alpha （TNF-α） in the supernatant of co-cultured cells. Results There was no significant difference in the mRNA of CD89 on neutrophils between the patients with HSP and healthy controls （P = 0.98）, but the protein of CD89 was significantly lower in the patients with HSP than in the healthy controls （0.60 ± 0.16 vs. 0.83 ± 0.24, P = 0.03）. The of CD11b on neutrophils was significantly higher in the patients with HSP than in the healthy controls （1 880.25 ± 388.29 vs. 1 109.25 ± 364.25, P < 0.01）. The apoptosis rate of co-cultured HUVEC was also significantly higher in the HSP group than in the healthy control group （37.44% ± 5.49% vs. 17.14% ± 4.45%, P < 0.01）. In addition, the HSP IgA group showed significantly higher apoptosis rate of co-cultured HUVEC and levels of IL-8 and TNF-α in the supernatant compared with the mIgA group （all P < 0.01） and blank control group （P < 0.01, = 0.01, = 0.02, respectively）. Conclusions Peripheral blood neutrophils in patients with HSP are activated, which can induce the apoptosis of vascular endothelial cells. HSP IgA can promote the neutrophil-mediated apoptosis of vascular endothelial cells and secretion of IL-8 and TNF-α, while mIgA may show a certain inhibitory effects.