HSP Pathogenesis

HSP is a common systemic childhood vasculitis, characterized by peripheral leucocytosis and polymorphonuclear neutrophils (PMNs) infiltration around the blood vessel.3 Although the etiology of HSP is not fully understood, genetic factors and activation of cellular immune response might play fundamental roles in HSP pathogenesis. IL-8, as an important chemokine that can both initiate and amplify the acute inflammatory responses, has been reported to be involved in the pathogenesis of some autoimmune and inflammatory diseases. In this regard, it has been demonstrated that the serum level of IL-8 in HSP group was significantly higher than controls,9,15 and this in part contributed to leucocytosis and PMNs infiltration around vessels in HSP.9 Furthermore, CAAT/enhancer binding protein β preferentially binds in the presence of the IL-8 gene +781T allele, which can promote IL-8 gene transcription and regulation.29,36 Thus, we speculate that individuals …show more content…
Risk assessment found that there was not a significant risk for HSP if the patient is with TT genotype (OR: 1.11, 95% CI: 0.61-2.03) or with CT genotype (OR: 0.82, 95% CI: 0.53-1.26). Patients with the 2767 A allele showed higher proteinuria and creatinine levels at follow-up.31 Yet, proteinuria and the serum level of creatinine in the acute stage of HSP had no relationship with IL-8 gene +781C/T polymorphism in this study. The TT genotype frequencies of the IL-8 gene +781C/T polymorphism in HSP patients with renal, GI and arthritis manifestations were 17.4%, 15.7%, and 18.6%, respectively. No significant differences in the distribution of genotype frequencies of IL-8 gene +781 C/T polymorphism were found between the controls and HSP patient subgroups. IL-8 gene +781 C/T polymorphism did not seem to have an impact on the development of renal, GI and arthritis manifestations of the