重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2015年
3期
293-294,298
,共3页
螺杆菌 ,幽门%胃黏膜%细胞因子类%感染
螺桿菌 ,幽門%胃黏膜%細胞因子類%感染
라간균 ,유문%위점막%세포인자류%감염
Helicobacter pylori%gastric mucosa%cytokines%infection
目的:研究幽门螺旋杆菌(简称幽门螺杆菌)感染小鼠胃黏膜组织细胞因子变化,初步探讨幽门螺杆菌感染的免疫机制。方法选取8~10周龄BALB/c小鼠24只,雌雄各半,分为观察组和对照组,两组造模前均禁食12h,观察组以2×109CFU/mL浓度的幽门螺杆菌菌液0.5mL/d灌胃,连续7d。对照组灌胃给生理盐水,0.5mL/d,连续7d,进行幽门螺杆菌感染小鼠胃黏膜造模。采用实时定量荧光PCR(Real‐timePCR)检测检测感染2、4周后,小鼠血浆中γ干扰素(IFN‐γ)、重组改构人肿瘤坏死因子α(TNF‐α)、白细胞介素‐8(IL‐8)以及IL‐10mRNA的表达量,并于感染4周后,处死小鼠,无菌取各组小鼠的胃组织,采用酶联免疫吸附试验夹心法检测胃黏膜组织中IFN‐γ、TNF‐α、IL‐8及IL‐10蛋白的水平。结果两组小鼠感染2周后,观察组IL‐8高于对照组,差异有统计学意义(P<0.05)。感染4周后,IFN‐γ、TNF‐α、IL‐8的mRNA及蛋白表达量均明显上升,但观察组上升幅度明显高于对照组,差异有统计学意义(P<0.05)。结论TH2细胞在幽门螺杆菌感染中的作用表现不明显,能促进TH1型细胞细胞因子的表达,引发TH1为主的免疫反应。
目的:研究幽門螺鏇桿菌(簡稱幽門螺桿菌)感染小鼠胃黏膜組織細胞因子變化,初步探討幽門螺桿菌感染的免疫機製。方法選取8~10週齡BALB/c小鼠24隻,雌雄各半,分為觀察組和對照組,兩組造模前均禁食12h,觀察組以2×109CFU/mL濃度的幽門螺桿菌菌液0.5mL/d灌胃,連續7d。對照組灌胃給生理鹽水,0.5mL/d,連續7d,進行幽門螺桿菌感染小鼠胃黏膜造模。採用實時定量熒光PCR(Real‐timePCR)檢測檢測感染2、4週後,小鼠血漿中γ榦擾素(IFN‐γ)、重組改構人腫瘤壞死因子α(TNF‐α)、白細胞介素‐8(IL‐8)以及IL‐10mRNA的錶達量,併于感染4週後,處死小鼠,無菌取各組小鼠的胃組織,採用酶聯免疫吸附試驗夾心法檢測胃黏膜組織中IFN‐γ、TNF‐α、IL‐8及IL‐10蛋白的水平。結果兩組小鼠感染2週後,觀察組IL‐8高于對照組,差異有統計學意義(P<0.05)。感染4週後,IFN‐γ、TNF‐α、IL‐8的mRNA及蛋白錶達量均明顯上升,但觀察組上升幅度明顯高于對照組,差異有統計學意義(P<0.05)。結論TH2細胞在幽門螺桿菌感染中的作用錶現不明顯,能促進TH1型細胞細胞因子的錶達,引髮TH1為主的免疫反應。
목적:연구유문라선간균(간칭유문라간균)감염소서위점막조직세포인자변화,초보탐토유문라간균감염적면역궤제。방법선취8~10주령BALB/c소서24지,자웅각반,분위관찰조화대조조,량조조모전균금식12h,관찰조이2×109CFU/mL농도적유문라간균균액0.5mL/d관위,련속7d。대조조관위급생리염수,0.5mL/d,련속7d,진행유문라간균감염소서위점막조모。채용실시정량형광PCR(Real‐timePCR)검측검측감염2、4주후,소서혈장중γ간우소(IFN‐γ)、중조개구인종류배사인자α(TNF‐α)、백세포개소‐8(IL‐8)이급IL‐10mRNA적표체량,병우감염4주후,처사소서,무균취각조소서적위조직,채용매련면역흡부시험협심법검측위점막조직중IFN‐γ、TNF‐α、IL‐8급IL‐10단백적수평。결과량조소서감염2주후,관찰조IL‐8고우대조조,차이유통계학의의(P<0.05)。감염4주후,IFN‐γ、TNF‐α、IL‐8적mRNA급단백표체량균명현상승,단관찰조상승폭도명현고우대조조,차이유통계학의의(P<0.05)。결론TH2세포재유문라간균감염중적작용표현불명현,능촉진TH1형세포세포인자적표체,인발TH1위주적면역반응。
Objective To study the change of cytokines in gastric mucosa of mice with Helicobacter pylori infection and explore the immune mechanism .Methods Twenty‐four 8-10 weeks‐old BALB/c mice were randomly divided into observation group and control group .After first 12 hours of fasting ,observation group was given 0 .5 mL/d Helicobacter pylori bacterial liquid with con‐centration of 2 × 109 CFU/mL for 7 consecutive days .The control group was fed with 0 .5 mL/d saline for 7 consecutive days .Then the mice were infected with Helicobacter pylori gast model was established .Using Real‐time PCR to detect the expressions of IFN‐γ ,TNF‐α,IL‐8 and IL‐10 in murine plasma within 2 ,4 weeks after infection .And after 4 weeks of infection ,mice were sacrificed , and their stomach tissue sterile were separated .ELISA was used to detect the levels of IFN‐γ,TNF‐α,IL‐8 ,and IL‐10 mRNA in gastric mucosa .Results There was significantly difference between groups 2 weeks after infection(P<0 .05) .With lastingness of infection ,the expression and the mRNA of IFN‐γ,TNF‐α,IL‐8 were significantly increased ,and the rate of increase of observation group was higher(P<0 .05) .Conclusion TH2 cells may have no effect on Helicobacter pylori infection in mice gastric mucosa and promote the expression of T H1‐type cytokines ,triggering immune response of T H1 .