解淀粉芽孢杆菌%BALB/c小鼠%肺炎%白介素8%白介素33%肿瘤坏死因子α%核因子κB p65
解澱粉芽孢桿菌%BALB/c小鼠%肺炎%白介素8%白介素33%腫瘤壞死因子α%覈因子κB p65
해정분아포간균%BALB/c소서%폐염%백개소8%백개소33%종류배사인자α%핵인자κB p65
Bacillus amyloliquefacien%BALB/c mice%Pneumonia%Interleukin-8%Interleukin-33%Tumor necrosis factor-α%Nuclear factor-κB p65
目的 建立解淀粉芽孢杆菌导致BALB/c小鼠肺炎模型,观察IL-8、IL-33、肿瘤坏死因子α(TNF-α)、核因子κB(NF-κB) p65的表达水平.方法 24只无特定病原体级雌性BALB/c小鼠随机分为空白对照组、实验组和免疫抑制组,每组分为3小组,每小组8只.实验组、免疫抑制组接种同浓度解淀粉芽孢杆菌菌悬液,空白对照组接种50 μl0.9％氯化钠.接种后第7天分批处死动物,观察其BALF中IL-8、IL-33、TNF-α表达,以及BALF和肺组织中NF-κB p65表达水平.结果 实验组IL-8水平与空白对照组比较,差异有统计学意义(t=4.53,P＜0.01);实验组IL-33水平与空白对照组比较,差异有统计学意义(t=2.99,P＜0.01);实验组TNF-α水平与空白对照组比较,差异有统计学意义(t=8.56,P＜0.01).免疫抑制组IL-8水平与空白对照组比较,差异有统计学意义(t=8.22,P＜0.01);免疫抑制组IL-33水平与空白对照组比较,差异有统计学意义(t=5.53,P＜0.01);免疫抑制组TNF-α水平与空白对照组比较,差异有统计学意义(t=7.21,P＜0.01).免疫抑制组IL-8水平与实验组比较,差异有统计学意义(t=4.53,P＜0.01);免疫抑制组IL-33水平与实验组比较,差异有统计学意义(t=2.89,P＜0.01);免疫抑制组TNF-α水平与实验组比较,差异有统计学意义(t =4.99,P＜0.01).免疫组织化学NF-κB p65水平:免疫抑制组NF-κB p65水平与空白对照组比较,差异有统计学意义(t=5.369,P＜0.05);实验组NF-κB p65水平与空白对照组比较,差异有统计学意义(t=3.507,P＜0.05);免疫抑制组NF-κB p65水平与实验组比较,差异有统计学意义(t=2.566,P＜0.05).Western blotting NF-κB p65水平:实验组NF-κB p65水平与空白对照组比较,差异有统计学意义(t=6.039,P＜0.01);免疫抑制组与空白对照组比较,差异有统计学意义(t =9.951,P＜0.01);免疫抑制组与实验组比较,差异有统计学意义(t=6.423,P＜0.01).结论 IL-8、IL-33、TNF-α、NF-κB p65参与了解淀粉芽孢杆菌致BALB/c小鼠肺炎的发生与发展.
目的 建立解澱粉芽孢桿菌導緻BALB/c小鼠肺炎模型,觀察IL-8、IL-33、腫瘤壞死因子α(TNF-α)、覈因子κB(NF-κB) p65的錶達水平.方法 24隻無特定病原體級雌性BALB/c小鼠隨機分為空白對照組、實驗組和免疫抑製組,每組分為3小組,每小組8隻.實驗組、免疫抑製組接種同濃度解澱粉芽孢桿菌菌懸液,空白對照組接種50 μl0.9％氯化鈉.接種後第7天分批處死動物,觀察其BALF中IL-8、IL-33、TNF-α錶達,以及BALF和肺組織中NF-κB p65錶達水平.結果 實驗組IL-8水平與空白對照組比較,差異有統計學意義(t=4.53,P＜0.01);實驗組IL-33水平與空白對照組比較,差異有統計學意義(t=2.99,P＜0.01);實驗組TNF-α水平與空白對照組比較,差異有統計學意義(t=8.56,P＜0.01).免疫抑製組IL-8水平與空白對照組比較,差異有統計學意義(t=8.22,P＜0.01);免疫抑製組IL-33水平與空白對照組比較,差異有統計學意義(t=5.53,P＜0.01);免疫抑製組TNF-α水平與空白對照組比較,差異有統計學意義(t=7.21,P＜0.01).免疫抑製組IL-8水平與實驗組比較,差異有統計學意義(t=4.53,P＜0.01);免疫抑製組IL-33水平與實驗組比較,差異有統計學意義(t=2.89,P＜0.01);免疫抑製組TNF-α水平與實驗組比較,差異有統計學意義(t =4.99,P＜0.01).免疫組織化學NF-κB p65水平:免疫抑製組NF-κB p65水平與空白對照組比較,差異有統計學意義(t=5.369,P＜0.05);實驗組NF-κB p65水平與空白對照組比較,差異有統計學意義(t=3.507,P＜0.05);免疫抑製組NF-κB p65水平與實驗組比較,差異有統計學意義(t=2.566,P＜0.05).Western blotting NF-κB p65水平:實驗組NF-κB p65水平與空白對照組比較,差異有統計學意義(t=6.039,P＜0.01);免疫抑製組與空白對照組比較,差異有統計學意義(t =9.951,P＜0.01);免疫抑製組與實驗組比較,差異有統計學意義(t=6.423,P＜0.01).結論 IL-8、IL-33、TNF-α、NF-κB p65參與瞭解澱粉芽孢桿菌緻BALB/c小鼠肺炎的髮生與髮展.
목적 건립해정분아포간균도치BALB/c소서폐염모형,관찰IL-8、IL-33、종류배사인자α(TNF-α)、핵인자κB(NF-κB) p65적표체수평.방법 24지무특정병원체급자성BALB/c소서수궤분위공백대조조、실험조화면역억제조,매조분위3소조,매소조8지.실험조、면역억제조접충동농도해정분아포간균균현액,공백대조조접충50 μl0.9％록화납.접충후제7천분비처사동물,관찰기BALF중IL-8、IL-33、TNF-α표체,이급BALF화폐조직중NF-κB p65표체수평.결과 실험조IL-8수평여공백대조조비교,차이유통계학의의(t=4.53,P＜0.01);실험조IL-33수평여공백대조조비교,차이유통계학의의(t=2.99,P＜0.01);실험조TNF-α수평여공백대조조비교,차이유통계학의의(t=8.56,P＜0.01).면역억제조IL-8수평여공백대조조비교,차이유통계학의의(t=8.22,P＜0.01);면역억제조IL-33수평여공백대조조비교,차이유통계학의의(t=5.53,P＜0.01);면역억제조TNF-α수평여공백대조조비교,차이유통계학의의(t=7.21,P＜0.01).면역억제조IL-8수평여실험조비교,차이유통계학의의(t=4.53,P＜0.01);면역억제조IL-33수평여실험조비교,차이유통계학의의(t=2.89,P＜0.01);면역억제조TNF-α수평여실험조비교,차이유통계학의의(t =4.99,P＜0.01).면역조직화학NF-κB p65수평:면역억제조NF-κB p65수평여공백대조조비교,차이유통계학의의(t=5.369,P＜0.05);실험조NF-κB p65수평여공백대조조비교,차이유통계학의의(t=3.507,P＜0.05);면역억제조NF-κB p65수평여실험조비교,차이유통계학의의(t=2.566,P＜0.05).Western blotting NF-κB p65수평:실험조NF-κB p65수평여공백대조조비교,차이유통계학의의(t=6.039,P＜0.01);면역억제조여공백대조조비교,차이유통계학의의(t =9.951,P＜0.01);면역억제조여실험조비교,차이유통계학의의(t=6.423,P＜0.01).결론 IL-8、IL-33、TNF-α、NF-κB p65삼여료해정분아포간균치BALB/c소서폐염적발생여발전.
Objective To establish bacterial pneumonia model of BALB/c mice caused by bacillus amyloliquefacien and to investigate expression levels of IL-8,IL 33,TNF-α in bronchoalveolar lavage fluid (BALF) and NF-κB p65 in lung tissue of the mice and BALF.Methods A total of 24 BALB/c mice were randomly divided into three groups: control group (n =8), experimental group (n =8), and immunocompromised group (n =8).Mice in the experimental group and the immunocompromised group were intratracheally injected with suspension of Bacillus amyloliquefaciens at the same concentration.Mice in the control group were intratracheaily injected with 50 μl saline.On the 7 day after, 8 mice of each group were killed to determine the concentration of IL-8, IL-33, TNF-α in BALF and NF-κB p65 in lung tissue of the mice and BALF.Results In the level of IL-8, IL-33,TNF-α of the experimental group was significantly higher than in the control (t =4.53, P ＜0.01;t =2.99, P ＜0.01;t =8.56, P ＜0.01).The immunosuppression group was also significantly higher than the control (t =8.22, P ＜0.01;t =5.53, P ＜ 0.01;t =7.21, P ＜ 0.01), futhermore the immunosuppression group was more significant than the experimental (t =4.53, P＜0.01;t =2.89, P ＜0.01;t =4.99, P ＜0.01).About variation of NF-κB p65 the experimental group was higher than control (t =3.507, P ＜0.05;t =6.039, P ＜0.01),the immunosuppression group was also significantly higher than control (t =5.369, P ＜ 0.05;t =9.951, P ＜ 0.01), moreover the immunosuppression group was higher than the experimental (t =2.566, P ＜0.05;t = 6.423, P ＜ 0.01).Conclusions Bacillus amyloliquefacien may play an important role in the pathogenesis and develop to pneumonia in experimental and immunosuppression group.The level of cytokines and the expression of NF-κB p65 in lung tissues of each group were statistically significant,explain the role of cytokines and NF-κB p65 between pneumonia and inflammation mechanism.
