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目的研究瘦素在猪螺杆菌(Helicobacter suis,H.suis)感染后胃黏膜相关淋巴样组织(mucosa-associated lymphoid tissue,MALT)形成中的作用及其可能的机制。方法 C57BL/6野生型小鼠、瘦素缺陷(Ob/Ob)小鼠各20只随机分为以下四组:正常小鼠未感染组(WT组)、正常小鼠H.suis感染组(WT+HS组)、Ob/Ob小鼠未感染组(Ob组)、Ob/Ob小鼠H.suis感染组(Ob+HS组),每组10只,感染12周后处死,收集小鼠血清与胃组织。采用HE染色检测各组小鼠胃黏膜淋巴滤泡的数量与大小;酶联免疫吸附测定(ELISA)检测各组小鼠血清中瘦素的浓度;实时荧光定量PCR检测各组小鼠胃黏膜中瘦素及其受体Ob-R、炎症因子IFN-γ及趋化因子CXCL13 mRNA表达水平。结果正常小鼠感染H.suis后可见胃黏膜淋巴滤泡形成;与WT+HS组相比,Ob+HS组小鼠血清及胃黏膜中均未检测到瘦素的表达,胃黏膜中未观察到淋巴滤泡形成,且IFN-γ与CXCL13 mRNA表达水平明显降低;体外实验结果发现,瘦素可刺激淋巴瘤B细胞分泌表达IFN-γ。结论瘦素可能通过促进H.suis感染后胃黏膜IFN-γ的表达参与了胃MALT的形成。
Objective To investigate the role of leptin in the formation of gastric mucosa-associated lymphoid tissue (MALT) after Helicobacter suis (H.suis) infection and its possible mechanism. Methods Twenty mice in C57BL / 6 wild type and Ob / Ob mice were randomly divided into the following four groups: untreated group (WT group), normal group (WT group), WT (Ob + Ob group) and Ob / Ob mice (Ob + HS group), 10 mice in each group. After 12 weeks of infection, mice were sacrificed and the serum of mice was collected With stomach tissue. The number and size of gastric mucosal lymphoid follicles in each group were detected by HE staining. The concentration of leptin in serum was detected by enzyme-linked immunosorbent assay (ELISA) Leptin and its receptor Ob-R, inflammatory cytokine IFN-γ and chemokine CXCL13 mRNA expression levels. Results Gastric mucosal lymphatic follicle formation was observed in normal mice infected with H.suis. Compared with WT + HS group, no leptin expression was detected in serum and gastric mucosa of Ob + HS group, but not in gastric mucosa To lymphoid follicles, and IFN-γ and CXCL13 mRNA expression levels were significantly reduced; in vitro experiments found that leptin can stimulate lymphoma B cells to secrete IFN-γ. Conclusion Leptin may be involved in the formation of gastric MALT by promoting the expression of IFN-γ in gastric mucosa after H.suis infection.