安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
Acta Universitatis Medicinalis Anhui
2015年
9期
1252-1258
,共7页
王云%黄升海%吴璇%李振兴%于莉%汪旻旻
王雲%黃升海%吳璇%李振興%于莉%汪旻旻
왕운%황승해%오선%리진흥%우리%왕민민
呼吸道合胞病毒%肺炎克雷伯菌%肺炎%TLR4%NF-κB%炎性因子
呼吸道閤胞病毒%肺炎剋雷伯菌%肺炎%TLR4%NF-κB%炎性因子
호흡도합포병독%폐염극뢰백균%폐염%TLR4%NF-κB%염성인자
respiratory syncytial virus%Klebsiella pneumonia%pneumonia%TLR4%NF-κB%inflammatory cytokines
目的 探讨呼吸道合胞病毒( RSV)合并肺炎克雷伯菌( Kp)感染SD大鼠后,初步研究其所致肺炎与TLR4-NF-κB信号转导通路的关系. 方法 60只雄性SD大鼠随机分为正常对照组、RSV组、Kp组及RSV+Kp组,以RSV、Kp滴鼻感染SD大鼠,分别于感染后第0、1、3、5、7天不同时间点,测量其体重、肺指数( LI )的变化;HE染色观察肺的病理学改变;RT-PCR法检测肺组织中TLR4、NF-κB的mRNA表达;Western blot检测NF-κB蛋白的表达;ELISA法检测肿瘤坏死因子-α( TNF-α)和白细胞介素-1β( IL-1β)含量的变化.结果 与正常对照组相比,RSV组和Kp组均存在弥漫性肺泡间隔增厚和炎症细胞浸润,且随感染时间的延长,肺泡结构破坏逐渐加重, LI、TLR4 mRNA、NF-κB mRNA、NF-κB 蛋白、TNF-α和IL-1β的表达均升高,并与RSV和Kp感染之间存在时间依赖性关系;RSV+Kp组 LI、TLR4 mRNA、NF-κB mRNA、NF-κB蛋白、TNF-α和IL-1β的表达量进一步升高,肺组织炎症明显加剧. 结论 RSV和Kp混合感染具有协同作用,加重肺部炎症;RSV合并Kp感染可能通过 TLR4-NF-κB途径诱导肺部炎症反应,释放细胞因子TNF-α和IL-1β等.
目的 探討呼吸道閤胞病毒( RSV)閤併肺炎剋雷伯菌( Kp)感染SD大鼠後,初步研究其所緻肺炎與TLR4-NF-κB信號轉導通路的關繫. 方法 60隻雄性SD大鼠隨機分為正常對照組、RSV組、Kp組及RSV+Kp組,以RSV、Kp滴鼻感染SD大鼠,分彆于感染後第0、1、3、5、7天不同時間點,測量其體重、肺指數( LI )的變化;HE染色觀察肺的病理學改變;RT-PCR法檢測肺組織中TLR4、NF-κB的mRNA錶達;Western blot檢測NF-κB蛋白的錶達;ELISA法檢測腫瘤壞死因子-α( TNF-α)和白細胞介素-1β( IL-1β)含量的變化.結果 與正常對照組相比,RSV組和Kp組均存在瀰漫性肺泡間隔增厚和炎癥細胞浸潤,且隨感染時間的延長,肺泡結構破壞逐漸加重, LI、TLR4 mRNA、NF-κB mRNA、NF-κB 蛋白、TNF-α和IL-1β的錶達均升高,併與RSV和Kp感染之間存在時間依賴性關繫;RSV+Kp組 LI、TLR4 mRNA、NF-κB mRNA、NF-κB蛋白、TNF-α和IL-1β的錶達量進一步升高,肺組織炎癥明顯加劇. 結論 RSV和Kp混閤感染具有協同作用,加重肺部炎癥;RSV閤併Kp感染可能通過 TLR4-NF-κB途徑誘導肺部炎癥反應,釋放細胞因子TNF-α和IL-1β等.
목적 탐토호흡도합포병독( RSV)합병폐염극뢰백균( Kp)감염SD대서후,초보연구기소치폐염여TLR4-NF-κB신호전도통로적관계. 방법 60지웅성SD대서수궤분위정상대조조、RSV조、Kp조급RSV+Kp조,이RSV、Kp적비감염SD대서,분별우감염후제0、1、3、5、7천불동시간점,측량기체중、폐지수( LI )적변화;HE염색관찰폐적병이학개변;RT-PCR법검측폐조직중TLR4、NF-κB적mRNA표체;Western blot검측NF-κB단백적표체;ELISA법검측종류배사인자-α( TNF-α)화백세포개소-1β( IL-1β)함량적변화.결과 여정상대조조상비,RSV조화Kp조균존재미만성폐포간격증후화염증세포침윤,차수감염시간적연장,폐포결구파배축점가중, LI、TLR4 mRNA、NF-κB mRNA、NF-κB 단백、TNF-α화IL-1β적표체균승고,병여RSV화Kp감염지간존재시간의뢰성관계;RSV+Kp조 LI、TLR4 mRNA、NF-κB mRNA、NF-κB단백、TNF-α화IL-1β적표체량진일보승고,폐조직염증명현가극. 결론 RSV화Kp혼합감염구유협동작용,가중폐부염증;RSV합병Kp감염가능통과 TLR4-NF-κB도경유도폐부염증반응,석방세포인자TNF-α화IL-1β등.
Objective This study investigates SD rats infected with pneumonia respiratory syncytial virus ( RSV) combined with klebsiella pneumonia ( Kp ) to explore its relationship with TLR4-NF-κB signal transduction path-way. Methods A total of 60 SD rats were divided into four groups randomly:control group, RSV group, Kp group and Kp + RSV group. All animals were infected with RSV or Kp using intranasal method. We observed the weights, lung index, histopathological changes in the lung tissues by HE staining, the expression of TLR4, NF-κB mRNA with RT-PCR, NF-κB protein by Western blot analysis in the lung tissues and the concentrations of TNF-α, IL-1β with ELISA at 0,1,3,5,7 days after RSV or Kp post-infections. Results Compared with control group,dif-fuse thickening of alveolar interval and inflammatory cells infiltration were observed in RSV and Kp group,and with the extension of infection time, the infection alveolar structure increased gradually. The expression of LI,TLR4 mR-NA,NF-kB mRNA,NF-kB protien,TNF-α and IL-1β increased and the relationship between RSV and Kp showed time dependence;in RSV + Kp group , the expression of LI, TLR4 mRNA, NF-kB mRNA, NF-kB protein, TNF-αand IL-1β increased gradully and lung tissue inflammation increased significantly. Conclusion RSV combined with Kp infection has synergistic effects and aggravates pulmonary inflammation. RSV combined with Kp infection can induce pulmonary defence cells release cytokines TNF-α and IL-1β by TLR4-NF-κB signal transduction path-way.