Effects of Streptococcus pneumoniae on the ultrastructure of alveolar epithelial cells type Ⅱ in the lung tissues of mice and children.
- Author:
Lin-Hua SHU
1
;
Yun-Xiao SHANG
;
Fu-Hui ZHANG
;
Han ZHANG
;
Xiao-Xue MA
;
Nan YANG
;
Wan-Jie HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Child; Epithelial Cells; ultrastructure; Female; Humans; Mice; Pneumonia, Pneumococcal; pathology; Pulmonary Alveoli; ultrastructure
- From: Chinese Journal of Contemporary Pediatrics 2011;13(4):336-339
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODSThe 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.
RESULTSQuantitative 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.
CONCLUSIONSS.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.