肺炎链球菌对小鼠及儿童肺泡Ⅱ型上皮细胞超微结构的影响

Effects of Streptococcus pneumoniae on the ultrastructure of alveolar epithelial cells type Ⅱ in the lung tissues of mice and children

目的研究肺炎链球菌(S.p)对昆明幼鼠和肺炎患儿肺泡Ⅱ型上皮细胞(AEC-Ⅱ)超微结构的影响,探究肺组织坏死的可能机制。方法将从1例肺炎链球菌坏死性肺炎(PNP)患儿血中培养的S.p混悬液(CFU:1×108/L)0.3 mL注入昆明幼鼠的主支气管中(肺炎组),将等量生理盐水注入对照组鼠的主支气管内。92 h后处死,取鼠右肺下叶肺组织(1 mm3)于2.5%的戊二醛中固定。该患儿行左下肺叶肺空洞切除时,将坏死和正常的肺组织标本(1 mm3)置于2.5%的戊二醛中固定。用透射电子显微镜观察鼠与患儿AEC-Ⅱ超微结构。结果在S.p作用下幼鼠与患儿AEC-Ⅱ的微绒毛减少,脱落。板层小体体积增大,排空加强,密度减低。线粒体数量减少。细胞核染色质浓缩,分布不均。结论 S.p作用下幼鼠与患儿AEC-Ⅱ损伤变化相一致。AEC-Ⅱ超微结构的损伤可能是S.p导致肺组织坏死的重要原因之一。[中国当代儿科杂志,2011,13(4):336-339]

Objective To explore the possible mechanisms of lung necrosis by examining the effects of Streptoccus pneumoniae（S.p） on the ultrastructure of alveolar epithelial cells type Ⅱ（AEC-Ⅱ） in the lung tissues of mice and children.Methods The suspended solutions of S.p strains cultured from the blood of a child with pneumococcal necrotizing pneumonia（PNP）（0.3 mL,CFU： 1×108/L） were instilled into the trachea of pathogen-free mice to prepare PNP model.The same amount of normal saline was given for the control group（10 mice）.The samples（1 mm3） from the lower lobe of right lung of the mice were obtained 92 hrs later and fixed in 2.5% glutaraldehyde.Normal and abnormal lung tissues（1 mm3） were obtained while operation for the left lower lobe pulmonary cavity excision in the child with PNP.The specimens were fixed in 2.5% glutaraldehyde and stored at 4℃.A transmission electron microscope was employed for the examination of the ultrastructure of AEC-Ⅱ in the lung tissues.Results Quantitative reduction and exfoliation of microvilli in S.p-infected AEC-Ⅱ were observed in both mice and this child compared with the control.Enlarged size,enhanced evacuation and reduced density of the lamellar bodies were also presented.The number of mitochondria was obviously reduced.The nucleolus chromatin concentrated and showed an inhomogeneous distribution.Conclusions S.p infection results in comparable damage to the ultrastructure of AEC-Ⅱ in mice and children that may represent one of the primary causes responsible for S.p-induced lung tissue necrosis.