title: CCL5, CXCL16, and CX3CL1 are associated with Henoch-Schonlein purpura.
abstract: Chemokines are involved in the pathogenesis of various vascular inflammations. However, information about chemokines in Henoch-Schonlein purpura (HSP) is limited. Herein, we investigated the serum CCL5, CXCL16, and CX3CL1 levels in HSP patients with controls and the ability of sera from HSP patients on chemokine production in human dermal microvascular endothelial cells. Enzyme-linked immunosorbent assay (ELISA) detected serum CCL5, CXCL16, and CX3CL1 levels in patients with HSP. Human dermal microvascular endothelial cell line (HMEC-1) was treated with sera from patients with HSP at different stages, patients with acute spontaneous urticaria, or controls. Serum levels of CCL5, CXCL16, and CX3CL1 were elevated in HSP patients at acute stage, which correlated with the severity of this disease. Sera from patients with active HSP markedly induced CCL5, CXCL16, and CX3CL1 production at both mRNA and protein levels. In addition, patients' sera-stimulated HMEC-1 supernatants enhanced HL-60 or THP-1 cells migration. Furthermore, patients' sera increased the phosphorylation of inhibitor of κB-α (IκBα) and phosphorylation of extracellular signal-regulated kinase (ERK)1/2 protein levels, upregulated the translocation of nuclear factor-κB (NF-κB) p65 to the nucleus. Taken together, we show firstly that CCL5, CXCL16, and CX3CL1 may be involved in the pathogenesis of HSP. Factors present in sera from patients with active HSP may act as an inducer of inflammatory response in HMEC-1 cells and contribute to chemokine production through NF-κB and ERK 1/2 pathways.
authors.affiliation: Department of Dermatovenereology, West China Hospital of Sichuan University, Chengdu, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Chen
authors.forename: Zai-Pei
authors.initials: ZP
authors.lastname: Guo
authors.forename: Xiao-Yan
authors.initials: XY
authors.lastname: Jiao
authors.forename: Rui-Zhen
authors.initials: RZ
authors.lastname: Jia
authors.forename: Yu-Hong
authors.initials: YH
authors.lastname: Zhang
authors.forename: Jing-Yi
authors.initials: JY
authors.lastname: Li
authors.forename: Xu-Lei
authors.initials: XL
authors.lastname: Huang
authors.forename: Hong-Jie
authors.initials: HJ
authors.lastname: Liu
authors.forename: Ting
authors.initials: T
authors.lastname: Lai
mesh_terms: D021581:Active Transport, Cell Nucleus; D002460:Cell Line; D002467:Cell Nucleus / Q000378:metabolism*; D018946:Chemokine CCL5 / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D054428:Chemokine CX3CL1 / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D000075743:Chemokine CXCL16; D019743:Chemokines, CXC / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D004730:Endothelium, Vascular / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism*; D011695:IgA Vasculitis / Q000097:blood / Q000276:immunology*; D020935:MAP Kinase Signaling System; D055806:Microvessels / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism*; D010766:Phosphorylation; D051116:Receptors, Scavenger / Q000096:biosynthesis / Q000097:blood / Q000235:genetics; D044967:Serum
chemical_list: C423727:CXCL16 protein, human; D018946:Chemokine CCL5; D054428:Chemokine CX3CL1; D000075743:Chemokine CXCL16; D019743:Chemokines, CXC; D020672:I-kappa B Proteins; D016328:NF-kappa B; D051116:Receptors, Scavenger