论文部分内容阅读
目的通过构建小鼠感染模型,研究幽门螺杆菌(Hp)感染对白细胞相关免疫球蛋白样受体-1(LAIR-1)表达的影响。方法将32只C57BL/6小鼠随机分为对照组和感染组。感染组通过Hp菌液灌胃建立小鼠感染模型,对照组以PBS灌胃。6周后处死小鼠,采用胃黏膜分离培养、革兰染色、PCR及生化反应检查Hp定植情况,采用流式细胞术检测小鼠外周血单个核细胞(PBMC)中单核细胞和淋巴细胞表面LAIR-1的表达。结果感染组小鼠Hp感染率为91.3%(21/23)。感染组和对照组小鼠PBMC中单核细胞比例分别为(22.85±3.56)%和(49.85±0.35)%,淋巴细胞比例分别为(40.93±10.05)%和(30.15±0.35)%,差异均有统计学意义(t=5.845和2.137,P<0.05)。感染组和对照组小鼠PBMC表面LAIR-1表达率分别为(70.16±7.75)%和(83.4±0.1)%,淋巴细胞表面LAIR-1表达率分别为(56.81±11.37)%和(72.3±0.6)%,差异均有统计学意义(t=3.761和2.491,P<0.05)。结论 Hp感染下调了小鼠PBMC中单核细胞及LAIR-1的表达,上调淋巴细胞比例但下调其LAIR-1的表达。
Objective To investigate the effect of Helicobacter pylori (Hp) infection on the expression of leukocyte associated immunoglobulin-like receptor-1 (LAIR-1) in mice by constructing a mouse model of infection. Methods 32 C57BL / 6 mice were randomly divided into control group and infected group. The infection group was established by intragastric administration of Hp bacteria intragastric infection model, the control group with PBS. After 6 weeks, the mice were sacrificed and the colonization of Hp was examined by Gram stain, PCR and biochemical reaction. The mononuclear cells and lymphocytes in peripheral blood mononuclear cells (PBMCs) were detected by flow cytometry LAIR-1 expression. Results The infection rate of Hp in infected mice was 91.3% (21/23). The percentage of monocytes in peripheral blood mononuclear cells (PBMCs) of infected and control mice were (22.85 ± 3.56)% and (49.85 ± 0.35)% respectively, and the percentage of lymphocytes were (40.93 ± 10.05)% and (30.15 ± 0.35)%, respectively Statistically significant (t = 5.845 and 2.137, P <0.05). The expression rates of LAIR-1 on the surface of PBMC of infected and control mice were (70.16 ± 7.75)% and (83.4 ± 0.1)%, respectively. The expression rates of LAIR-1 on lymphocytes were (56.81 ± 11.37)% and 0.6%), the differences were statistically significant (t = 3.761 and 2.491, P <0.05). Conclusions Hp infection down-regulated the expression of monocytes and LAIR-1 in PBMC of mice, up-regulated the proportion of lymphocytes but down-regulated the expression of LAIR-1.