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纸质出版:2014
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杨再兴,邱倩,焦燕,但小苹,熊玮.淋巴细胞微粒诱导的小鼠气道炎症模型的建立及评价[J].陆军军医大学学报(原第三军医大学学报),2014,36(07):678-681.
Yang Zaixing,Qiu Qian,Jiao Yan,Dan Xiaoping,Xiong Wei.Establishment and evaluation of a mouse model of airway inflammation by lymphocyte-derived microparticles[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(07):678-681.
杨再兴,邱倩,焦燕,但小苹,熊玮.淋巴细胞微粒诱导的小鼠气道炎症模型的建立及评价[J].陆军军医大学学报(原第三军医大学学报),2014,36(07):678-681. DOI:
Yang Zaixing,Qiu Qian,Jiao Yan,Dan Xiaoping,Xiong Wei.Establishment and evaluation of a mouse model of airway inflammation by lymphocyte-derived microparticles[J].J Amry Med Univ (J Third Mil Med Univ),2014,36(07):678-681. DOI:
目的 利用T淋巴细胞微粒诱导建立小鼠气道炎症模型,探讨淋巴细胞微粒在气道炎症发生中的作用。 方法 放线菌素D溶液处理6T-CEM细胞24 h,收集淋巴细胞微粒;50 μg/mL的淋巴细胞微粒灌注BALB/c小鼠气道,24 h 后处死小鼠并取肺组织;HE染色检测肺组织的形态变化,ELISA、Western blot和荧光定量PCR法分别检测免疫相关分子NLRP3、TLR4、IL-18和IL-1β的蛋白和mRNA表达水平。 结果 HE染色显示淋巴细胞微粒处理组小鼠肺泡细胞聚集且伴随淋巴细胞浸润,ELISA结果显示淋巴细胞微粒处理组小鼠肺组织中IL-18和IL-1β的蛋白分泌水平显著高于正常组 (
P
0.01),荧光定量PCR和Western blot结果显示处理组小鼠肺组织中NLRP3、TLR4、IL-18和IL-1β的mRNA和蛋白表达水平显著高于正常组 (
P
0.01)。 结论 淋巴细胞微粒能够诱导小鼠气道炎症反应,其炎症反应与NLRP3、TLR4、IL-18和IL-1β等因子有关。
Objective To establish a mouse model of airway inflammation induced by lymphocyte-derived microparticels (LMPs) and investigate the role of LMPs in the incidence of airway inflammation. Methods After human T-leukemia cell line 6T-CEM was treated with actinomycin D for 24 h
the LMPs were collected. A total of 12 BALB/c mice were divided into normal group and LMPs group (n=6)
and their airways were infused with 100 μL normal saline and 50 μg/mL LMPs respectively. In 24 h later
all mice were killed
and then the lung tissues were accessed. HE staining was used to analyz
e the morphological changes of lung tissues. ELISA
Western blotting and quantity RT-PCR assays were used to measure the expression of immune-related molecules
NLRP3
TLR4
IL-18 and IL-1β at protein and mRNA levels. Results HE staining revealed alveolar cells aggregation and lymphocytic infiltration in the lung tissues of LMPs-treated mice. ELISA showed that the secreted protein levels of IL-18 and IL-1β were significantly higher in the lung tissues in LMPs-treated mice than normal control (
P
0.01). Quantity RT-PCR and Western blot assays showed that the mRNA and protein expression of NLRP3
TLR4
IL-18 and IL-1β were significantly increased in the lung tissues in LMPs-treated mice than normal control (
P
0.01). Conclusion LMPs induce airway inflammation in mice
and the inflammatory response is related to NLRP3
TLR4
IL-18 and IL-1β.
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