| Objective To investigate the expression of interleukin-17(IL-17)and its related cytokines in peripheral blood and intestinal mucosa and their roles in the pathogenesis of abdominal Henoch-Schonlein Purpura(HSP)in children.Meanwhile,preliminarily explore the relationship between intestinal dysbacteriosis and the pathogenesis of abdominal HSP in children.Methods The peripheral blood and feces specimens of 26 children with abdominal HSP and 16 healthy children were collected from pediatrics department of the First Affiliated Hospital of Guangxi medical university from November 2015 to February 2018.And then devided into observation group and healthy control.On the other hand,the duodenal mucosal biopsies of 20 children with abdominal HSP diagnosed by gastroscopy and 8 without obvious mucosal lesions were collected.And then devided into case group and control.Next,flow cytometry(FCM)was used to detect the proportions of helper T cell-17(Th17cells)and cytotoxic T cell-17(Tc17 cells)in peripheral blood mononuclear cells(PBMCs);Enzyme-linked Immunosorbent Assay(ELISA)was conducted tomeasure the plasma cytokine concentrations of IL-17,IL-6,IL-23 and γ-interferon(IFN-γ);Histopathological changes of duodenal mucosa biopsy were observed by hematoxylin-eosin staining(HE staining);Reverse transcription quantitative polymerase chain reaction(RT-qPCR)was performed to evaluate the mRNA expression levels of IL-17,IL-6,IL-23 and IFN-γ in duodenal mucosa.Immunohistochemical staining was applied to evaluate the protein expression levels of IL-17,IL-6,IL-23 and IFN-γ in duodenal mucosa.Bacterial 16 S rDNA quantitative PCR(16S rDNA qPCR)was used to quantify the gene copy number(CN)of Bifidobacterium and Escherichia coli in feces pecimens.Results 1.The proportions of Th17 and Tc17 cells in PBMCs in observation group were significantly higher than those in healthy control(p <0.01).However,there was no significant difference between observation and healthy control groups for the ratio of Th17/Tc17 cells(P > 0.05).2.The plasma cytokine concentrations of IL-17,IL-6 and IL-23 in observation group were significantly higher than those in healthy control group(P < 0.05 and/or P <0.01),but no significant difference in IFN-γexpression was detected between the two groups(P > 0.05).3.The histopathological changes of duodenal mucosa in the case group were mainly characterized by non-specific chronic inflammatory changes such as mucosal congestion,edema,erosion,ulcer,etc.Mucosal vascular inflammatory lesions could be observed in some cases.4.The mRNA expression levels of IL-17,IL-6 and IFN-γin duodenal mucosa of the case group were significantly higher than those in the control group(P < 0.05and/or P < 0.01),while no significant difference of mRNA expression level of IL-23 was detected between the two groups(P > 0.05).5.Protein levels of IL-17,IL-6 and IFN-γin duodenal mucosa of the case group were significantly higherthan those in the control group(P < 0.01),but there was no significant difference in the protein level of IL-23 between the two groups(P > 0.05).6.The gene CN of Bifidobacterium and the ratio of Bifidobacterium/ Escherichia coli(B/E)in the observation group were significantly lower than those in the healthy control group(P < 0.01),while no significant difference in the gene CN of Escherichia coli was found between the two groups(P > 0.05).Conclusions 1.Th17 cells,Tc17 cells and IL-17,IL-6,IL-23,IFN-γmay be involved in the genesis and development of abdominal HSP in children.2.IL-17 and its related cytokines are involved in systemic and intestinal inflammation in children with abdominal HSP.3.Intestinal dysbacteriosis may be related to the inflammatory reaction mediated by IL-17,which is likely to involved in the pathogenesis of abdominal HSP and the damage of intestinal mucosal barrier in children. |