幽门螺杆菌感染对功能性消化不良病儿发病的影响

对照。结果FD病儿HP感染率（60%）显著高于健康对照儿童（15%），差异有显著性（χ2=43.2，P<0.01）。HP阳性组CagA阳性者占80%，与CagA阴性组、HP阴性组相比，CagA阳性组病儿的消化不良症状积分明显增高（F=91.26，q=6.73、19.08，P<0.01），胃黏膜炎症程度与炎性细胞浸润亦明显增加;血清5-羟色胺与瘦素水平明显降低，促胃液素与胃促生长素水平明显增高，差异均有显著意义（F=622.35～3 724.33，q=5.29～122.04，P<0.01）;胃组织中炎症因子IL-17、INF-γ与趋化因子CXCL13、CCL2的mRNA表达水平均显著增高，差异有统计学意义（F=413.72～842.75，q=16.11～57.98，P<0.01）。结论HP感染可能是儿童FD的重要致病因素之一;HP感染可能通过CagA的作用影响胃肠激素的分泌与局部黏膜免疫反應而参与FD的发病。

[关键词]消化不良;幽门螺杆菌;胃肠激素;趋化因子类

[中图分类号]R725.7[文献标志码]A[文章编号]2096-5532（2019）03-0257-05

[ABSTRACT]ObjectiveTo investigate the effect of Helicobacter pylori （HP） infection on the pathogenesis of functional dyspepsia （FD） in children. MethodsA total of 100 children diagnosed with FD were eolled. The severity of dyspepsia was determined and scored， and the 13C-urea breath test was performed to identify HP infection. According to the results of HP detection， the children with FD were divided into HP-positive group and HP-negative group. Based on the results of cytotoxin-associated protein A （CagA） antibody detection， the children in the HP-positive group were further divided into CagA-positive group and CagA-negative group. ELISA was used to measure the expression of related gastrointestinal hormones in serum. Gastroscopy was performed to collect gastric mucosa for HE staining， the degree of gastric mucosal inflammation was determined， and the infiltration of inflammatory cells was observed. Quantitative real-time PCR was used to measure the mRNA expression of associated inflammatory cytokines and chemokines in gastric mucosa. A total of 100 healthy children who underwent physical examination were eolled as healthy control group. ResultsThe children with FD had a significantly higher HP infection rate than the healthy children （60% vs 15%， χ2=43.2，P<0.01）. In the HP-positive group， the children with positive CagA accounted for 80%. Compared with the CagA-negative group and the HP-negative group， the CagA-positive group had a significantly higher symptom score of dyspepsia （F=91.26，q=6.73 and 19.08，P<0.01）， significant increases in the degree of gastric mucosal inflammation and the infiltration of inflammatory cells， significant reductions in the serum levels of 5-hydroxytryptamine  and leptin， and significant increases in the levels of gastrin and ghrelin （F=622.35-3 724.33，q=5.29-122.04，P<0.01）. Compared with the CagA-negative group and the HP-negative group， the CagA-positive group had significant increases in the mRNA expression of the inflammatory cytokines interleukin-17 and interferon-γ and the chemokines CXCL13 and CCL2 in gastric tissue （F=413.72-842.75，q=16.11-57.98，P<0.01）. ConclusionHP infection may be one of the important pathogenic factors for FD in children. HP infection may participate in the pathogenesis of FD by affecting the secretion of gastrointestinal hormones and local mucosal immune response via CagA.