高脂饮食性肥胖对猪螺杆菌感染后小鼠胃淋巴趋化因子表达与MALT形成的影响  

EFFECT OF HIGH-FAT DIET-INDUCED OBESITY ON GASTRIC LYMPHOCYTE CHEMOKINE EXPRESSION AND MUCOSA-ASSOCIATED LYMPHOID TISSUE FORMATION IN MICE AFTER HELICOBACTER SUIS INFECTION

作　　者：杨鑫 田字彬[1] 张翠萍[1] 张茜[1] 赵文君[1] 杨林[1] YANG Xin;TIAN Zibin;ZHANG Cuiping;ZHANG Qian;ZHAO Wenjun;YANG Lin(Department of Gastroenterology,The Affiliated Hospital of Qingdao University,Qingdao 266003,China)

机构地区：[1]青岛大学附属医院消化内科,山东青岛266003

出　　处：《青岛大学学报（医学版）》2020年第6期631-635,共5页Journal of Qingdao University(Medical Sciences)

基　　金：国家自然科学基金面上项目(81572320)。

摘　　要：目的研究高脂饮食性肥胖对猪螺杆菌感染后小鼠胃相关淋巴趋化因子表达与黏膜相关淋巴组织(MALT)形成影响及其机制。方法将40只雌性C57BL/6小鼠随机分为正常对照组(NC组)、猪螺杆菌感染组(HS组)、高脂饮食组(HFD组)、猪螺杆菌感染+高脂饮食组(HS+HFD组),每组10只。用普通饮食喂养NC组与HS组小鼠,而其余两组小鼠普通饮食喂养3周后给予高脂饮食。按上述饮食喂养24周后,取小鼠胃组织,行苏木精-伊红染色分别检测各组小鼠胃黏膜淋巴滤泡的数量与大小;行实时定量PCR,分别检测各组小鼠胃黏膜相关淋巴趋化因子CXCL13、CCL19、CCL21和核转录因子-κB(NF-κB)信号通路的上游因子肿瘤坏死因子α(TNF-α)、淋巴毒素α(LTα)、淋巴毒素β(LTβ)的mRNA表达水平。结果猪螺杆菌感染可诱导小鼠胃黏膜滤泡的形成,且HS+HFD组小鼠胃黏膜淋巴滤泡的数量与大小较HS组明显增加(t=3.05、4.01,P<0.05)。HS+HFD组小鼠胃黏膜中TNF-α、LTα与LTβ的mRNA表达水平与HS组相比较明显增加(F=117.261~306.855,P<0.05)。HS+HFD组小鼠胃黏膜相关淋巴趋化因子CXCL13、CCL19、CCL21的mRNA表达水平明显高于HS组,差异具有统计学意义(F=68.461~252.398,P<0.05)。结论高脂饮食诱导的肥胖可能通过激活NF-κB信号通路以及诱导上调胃内淋巴趋化因子表达,进一步促进猪螺杆菌感染后胃MALT的形成。ObjectiveTo investigate the effect of high-fat diet-induced obesity on the expression of gastric lymphocyte chemokines and the formation of mucosa-associated lymphoid tissue(MALT)after Helicobacter suis(H.suis)infection and its possible mechanism.MethodsA total of 40 female C57BL/6 mice were randomly divided into normal control group(NC group),H.suis infection group(HS group),high-fat diet group(HFD group),and H.suis infection+high-fat diet group(HS+HFD group),with 10 mice in each group.The mice in the NC group and the HS group were given a normal diet,and those in the other two groups were given high-fat diet after 3 weeks of normal diet.After the mice were given the above diet for 24 weeks,gastric tissue was collected and HE staining was used to measure the number and size of gastric mucosal lymphoid follicles;quantitative real-time PCR was used to measure the mRNA expression levels of gastric mucosa-associated lymphocyte chemokines(CXCL13,CCL19,and CCL21)and upstream factors of the nuclear factor-kappa B(NF-κB)signaling pathway(tumor necrosis factor-α(TNF-α),lymphotoxinα(LTα),and lymphotoxinβ(LTβ)).ResultsH.suis infection induced the formation of gastric mucosal follicles in mice,and the HS+HFD group had significantly greater number and size of gastric mucosal lymphoid follicles than the HS group(t=3.05,4.01;P<0.05).Compared with the HS group,the HS+HFD group had significant increases in the mRNA expression levels of TNF-α,LTα,and LTβin the gastric mucosa(F=117.261-306.855,P<0.05),as well as significantly higher mRNA expression levels of the gastric mucosa-associated lymphocyte chemokines CXCL13,CCL19,and CCL21(F=68.461-252.398,P<0.05).ConclusionHigh-fat diet-induced obesity may further promote the formation of gastric MALT after H.suis infection by activating the NF-κB signaling pathway and inducing upregulation of the expression of gastric lymphocyte chemokines.

关 键 词：小鼠 肥胖 膳食 高脂 海尔曼螺杆菌属 黏膜相关淋巴组织 趋化因子类 NF-κB 

分 类 号：R573.6[医药卫生—消化系统]