自噬真核细胞在不动杆菌清除中的机制及诱导巨噬细胞凋亡的蛋白质组织学研究

Mechanisms of autophagic eukaryotic cells in Acinetobacter microvilli removal and protein histological study on apoptosis induced by macrophages

目的观察自噬真核细胞在不动杆菌清除中的机制及对诱导巨噬细胞凋亡蛋白质组织学的影响。方法取OCR雌性小鼠24只,建立小鼠不动杆菌感染模型,随机分为对照组(n=12)和观察组(n=12)。对照组注射生理盐水,观察组注射自噬真核细胞,测定两组小鼠不动杆菌清除情况及诱导巨噬细胞凋亡的蛋白质组织学情况。结果两组小鼠植入后即刻病灶组织细菌定量比较,差异无统计学意义(P>0.05);观察组植入后24、48h病灶组织细菌定量,显著低于对照组(P<0.05);观察组小鼠注射自噬真核细胞后肺部组织基本正常,肺泡腔开放,未见异常物质,肺泡壁无明显增厚,且壁内未见炎性细胞浸润。对照组小鼠由于注射生理盐水缺乏不动杆菌清除能力导致肺部可见大量炎性细胞浸润,血管扩张,部分小鼠存在充血现象。结论不动杆菌小鼠体内注射自噬真核细胞能提高机体清除率,诱导巨噬细胞凋亡。

Objective To observe the mechanisms of autophagic eukaryotic cells in Acinetobacter microvilli removal and protein histological study on apoptosis induced by macrophages.Methods A model of Acinetobacter baumannii infection was established in 24 female OCR mice.The mice were randomly divided into control group （n=12） and observation group（n=12）.The control group was injected with normal saline,and the observation group was injected with autophagy eukaryotic cells,the histopathological changes of Acinetobacter and the induction of macrophage apoptosis were observed.Results There was no significant difference in the bacterial counts between the two groups of mice immediately after implantation （P〉0.05）,the bacterial counts in the 24 and 48 hin the observation group was significantly lower than that in the control group （P〈0.05）.The lung tissue of mice in the observation group injected after autophagy was normal,the alveolar cavity was open,no abnormal substances were found,the alveolar wall was not obviously thickened,and no inflammatory cell infiltration was found in the wall.The mice in the control group were injected with normal saline and lacked the ability to remove Acinetobacter,resulting in a large number of inflammatory cell infiltration,vasodilatation,and congestion in some mice.Conclusion Autophagic eukaryotic cells injected with Acinetobacter baumannii can increase the clearance rate,induce apoptosis of macrophages and improve the quality of Acinetobacter baumannii.