Effect Of IgAl Isolated From Henoch-Schonlein Purpura Patients On Inflammatory Mediators Production Of By Human Umbilical Venous Endothelial Cells

ObjectiveHenoch-Sch nlein purpura (HSP) is the most common vasculitis of childhood. Thepathogenesis of HSP is not clear although there is evidence to support that vascularendothelial cell injury was the pathological basis. Observe the changes of the cytokinewhen human umbilical venous endothelial cells (HUVECs) were induced by the seraand IgA1from Henoch-Sch nlein purpura (HSP) patients and the expression ofIntercellular adhesion molecule-1(ICAM-1) and nuclear factor-κB (NF-κB).To explorethe pathogenic mechanism of the injury on endothelial cell was caused by IgA1inchildren with HSP.Methods1. Ten children with HSP, admitted in the first Affiliated Hospital of Anhui MedicalUniversity,were enrolled in the Study. Ten normal healthy children were enrolled ascontrols. Serum samples were obtained from peripheral vein of all subjects in themorning. Serum IgA1was purified by jacalin affinity chromatography.2. HUVECs were divided into three groups based on the culture conditions:, HSPgroup,normal group, blank control group.HSP group: cultured with the sera and IgA1from HSP patients; normal group:cultured with the sera and IgA1from health chlidren; blank control group: cultured withRPMI-l640. The levels of inflammatory mediators in the supernatants of each group were detected after cultivation for12hs.The effects of different concentrations of IgA1on proliferation of HUVECsthrough MTT were observed.The expression of NF-κB and ICAM-1were detected by real time PCR andwestern blot.Results1. The levels of IL8, TNF-α,and NO in HSP group were significantly higher than blankcontrol group and normal serum group (P<0.05), after cultivation for12hs with thesera and IgA1.2. Both IgA1from HSP patient and healthy controls could promote the proliferation ofHUVECs in concentration dependent manner (P<0.05). At the same stimulatingconcentration, IgA1form HSP patient could combine with HUVECs more easilythan healthy control(P<0.05).3. The levels of NF-κB, ICAM-1mRNA in HSP group were significantly higher thannormal group (p<0.05) and blank control group (p<0.01). And compared theexpression of NF-κB, ICAM-1, the HSP group were also higher than other groups(p<0.01).Conclusion1. The IgA1from children with active HSP sera can induce the in vitro culturedHUVECs to become activated and excrete cytokines.2. The expression of inflammatory mediators up-regulated by IgA1through the NF-κBpathway may cause the injury on HUVECs.