黏附侵袭性大肠杆菌LF82对结肠炎小鼠炎症通路的影响  

Effect of adherent invasive Escherichia coli LF82 on intestinal inflammatory pathway in mice with colitis

作　　者：沙素梅 陈芬荣 涂永久 曾虹 景妍 崔婷 王晶[1] 李路[1] 徐斌 SHA Su-mei;CHEN Fen-rong;TU Yong-jiu;ZENG Hong;JING Yan;CUI Ting;WANG Jing;LI Lu;XU Bin(Department of Gastroenterology,the Second Affiliated Hospital of Xi′an Jiaotong University,Shannxi Provincial Key Laboratory of Gastrointestinal Motility Disorders,Shannxi Provincial Clinical Research Center of Gastrointestinal Diseases,Xi′an 710004,China;Department of General Surgery,the Chenggong Hospital Affiliated to Xiamen University(Central Hospital of the 73th Chinese People′s Liberation Army),Xiamen 361003,China)

机构地区：[1]西安交通大学第二附属医院消化内科、陕西省肠胃动力疾病研究重点实验室、陕西省胃肠疾病临床研究中心,710004 [2]厦门大学附属成功医院(陆军第73集团军医院)普通外科,361003

出　　处：《现代消化及介入诊疗》2021年第9期1108-1112,共5页Modern Interventional Diagnosis and Treatment in Gastroenterology

基　　金：陕西省自然科学基金青年项目(2021JQ-420);厦门市医疗卫生指导性项目(3502Z20209156)。

摘　　要：目的黏附侵袭性大肠杆菌(AIEC)可能与炎症性肠病(IBD)的发病及加重相关,本研究的目的是研究最具代表性的AIEC菌株E.coli LF82对实验性结肠炎小鼠炎症因子及炎症通路的影响。方法将24只清洁级C57BL/6小鼠随机分为DSS组、DSS+LF82组和健康对照组,每组8只。分别给予DSS组和DSS+LF82组小鼠蒸馏水和E.coli LF82灌胃一周,后建立葡聚糖硫酸钠(DSS)小鼠结肠炎模型,健康对照组小鼠不做任何处理。通过Bio-plex、real-time PCR和Western blot测定血清及结肠组织中多个炎症因子及炎症通路相关分子的变化。结果DSS组小鼠血清中的炎症因子肿瘤坏死因子-α、白介素-10、白介素-17A、白介素-1β、白介素-6、干扰素-γ和G-集落刺激因子分泌较健康对照组明显增加,定植E.coli LF82的DSS+LF82组升高更明显。结肠组织中的上述炎症因子和IL-8的mRNA水平变化趋势与之类似。DSS+LF82组小鼠结肠中磷酸化NF-κB P65和P38的表达明显高于DSS组和健康对照组。结论E.coli LF82可增加小鼠血清和结肠组织炎症因子的释放,其机制可能通过NF-κB和MAPK信号通路实现。Objective Adhesive invasive Escherichia coli(AIEC)may be related to the onset and exacerbation of inflammatory bowel disease(IBD).The aim of this study was to investigate the effects of the most representative AIEC strain E.coli LF82 on inflammatory cytokines and inflammatory response pathway related molecules in experimental colitis mice.Methods Twenty-four specific pathogen free(SPF)C57BL/6 mice were divided into DSS group,DSS+LF82 group and healthy control group,with 8 mice in each group.Mice in DSS group and DSS+LF82 group were given distilled water and E.coli LF82 by gavage for one week.Then the colitis model of dextran sulfate sodium(DSS)mice was established.Mice in healthy control group were not treated.Cytokine expression was measured by bio-plex in serum and by real-time polymerase chain reaction(PCR).NF-κB p65 and p38 were measured by western blot in colonic tissue.Results The levels of TNF-α,IL-10,IL-17A,IL-1β,IL-6,IFN-γand G-CSF in the serum of the DSS group and the DSS+LF82 group were significantly higher than those of the control group.The changes of TNF-α,IL-10,IL-17A,IL-1β,IL-6,IFN-γ,G-CSF and IL-8 mRNA in colon tissue were consistent with those in serum,which were more obvious in DSS+LF82 group.E.coli LF82 also induced the increasing of phosphorylation-NF-κB P65 and P38 in colon tissue.ConclusionAdministration of E.coli LF82 significantly increased mRNAs levels of cytokine in serum and colonic specimens.E.coli LF82 can exacerbate DSS-colitis in mice,the NF-κB and MAPK pathway maybe involved in the mechanism.

关 键 词：葡聚糖硫酸钠 黏附侵袭性大肠杆菌 结肠炎 炎症因子 

分 类 号：R574.6[医药卫生—消化系统]