白介素-1β在羊膜腔内注射脂多糖导致的新生鼠肺泡化阻滞中的作用

发布时间：2018-04-25 07:04

本文选题：白介素-β + 巨噬细胞　；参考：《上海交通大学学报(医学版)》2017年04期

【摘要】：目的·探讨白介素-1β(IL-1β)在羊膜腔内注射脂多糖(LPS)导致的新生鼠肺泡化阻滞中的作用。方法·通过SD孕鼠羊膜腔内注射LPS建立新生鼠支气管肺发育不良(BPD)模型。孕鼠(孕19 d)随机分为生理盐水(Saline)组、LPS组和LPS+anti-IL-1β组。随机取出生1、3、7 d新生鼠肺组织,经苏木精-伊红(H-E)染色后观察病理学改变,并通过real-time PCR和ELISA检测肺组织中IL-1βmRNA及蛋白表达水平。培养大鼠骨髓源性原代巨噬细胞,给予LPS干预,经全转录组测序检测与IL-1β相关的多个基因的表达变化。结果·与Saline组相比,LPS组肺泡和次级突起数量减少,平均内衬间隔增大;肺组织IL-1βmRNA表达及蛋白表达量均明显增加。应用anti-IL-1β可改善LPS引起的新生鼠肺组织病理变化。LPS可导致Gbp5、Ccl3、Nod2、Ccr5、Mefv、Casp4、Ifnar1等基因表达明显上调,而Lgals9、Gstp1基因表达明显下调,其中Gbp5、Ccl3、Nod2、Ccr5、Casp4、Ifnar1、Lgals9可正向调节IL-1β表达。结论·在BPD模型中LPS通过上调巨噬细胞中IL-1β的表达,诱导新生鼠肺泡化阻滞。全转录组测序揭示LPS可以通过多种路径调控巨噬细胞中IL-1β的表达。
[Abstract]:Objective to investigate the role of interleukin-1 尾 (IL-1 尾) in alveolar block induced by intraamniotic injection of lipopolysaccharide (LPS) in neonatal rats. Methods the neonatal model of bronchopulmonary dysplasia (BPD) was established by intraamniotic injection of LPS in SD pregnant rats. Pregnant rats were randomly divided into LPS anti-IL-1 尾 group and LPS anti-IL-1 尾 group. The lung tissues of neonatal rats were randomly selected for 7 days. The pathological changes were observed by hematoxylin-eosin H-E staining. The expression of IL-1 尾 mRNA and protein in lung tissue was detected by real-time PCR and ELISA. Rat bone marrow-derived primary macrophages were cultured and treated with LPS. The expression of multiple genes related to IL-1 尾 was detected by full transcriptional sequencing. Results compared with Saline group, the number of alveoli and secondary processes decreased, the average lining interval increased, and the expression of IL-1 尾 mRNA and protein in lung tissue increased significantly. The application of anti-IL-1 尾 could improve the pathological changes of lung tissue induced by LPS. LPs could induce the expression of Cbp5Ccl3Nod2 / Ccr5Efnar1, Caspase-4 and Ifnar1, but the expression of Lgals9 Gstp1 was down-regulated. Gbp5Ccl3Nod2Ccr5Casp4Ifnar1 / Lgals9 could positively regulate the expression of IL-1 尾. Conclusion in BPD model, LPS induces alveolar arrest by up-regulating the expression of IL-1 尾 in macrophages. Total transcriptional sequencing revealed that LPS could regulate the expression of IL-1 尾 in macrophages through multiple pathways.
【作者单位】：上海交通大学医学院附属新华医院新生儿科;上海市嘉定区中心医院儿科;
【分类号】：R722.1

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