Abstract 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.
SHU Lin-Hua,SHANG Yun-Xiao,ZHANG Fu-Hui et al. Effects of Streptococcus pneumoniae on the ultrastructure of alveolar epithelial cells type Ⅱ in the lung tissues of mice and children[J]. 中国当代儿科杂志, 2011, 13(4): 336-339.
SHU Lin-Hua,SHANG Yun-Xiao,ZHANG Fu-Hui et al. Effects of Streptococcus pneumoniae on the ultrastructure of alveolar epithelial cells type Ⅱ in the lung tissues of mice and children[J]. CJCP, 2011, 13(4): 336-339.
［1］Rudan I, Boschi-Pinto C, Biloglav Z, Mulholland K, Campbell H. Epidemiology and etiology of childhood pneumonia［J］. Bull World Health Organ, 2008, 86(5):408-416.
［2］Shibuya K, Fat DM. Background on Pneumonia［M］//Wardlaw T, Johansson EW, Hodge M. Pneumonia: The forgotten killer of children. UNICEF/WHO, 2006: 4-7.
［3］Sung H, Shin HB, Kim MN, Lee K, Kim EC, Song W, et al. Vancomycin-tolerant streptococcus pneumoniae in Korea［J］. J Clin Microbiol, 2006, 44(10): 3524-3528.
［7］Sawicki GS, Lu FL, Valim C, Cleveland RH, Colin AA. Necrotising pneumonia is an increasingly detected complication of pneumonia in children［J］. Eur Respir J, 2008, 31(6): 1285-1291.
［8］Bender JM, Ampofo K, Korgenski K, Daly J, Pavia AT, Mason EO, et al. pneumococcal necrotizing pneumonia in utah: does serotype matter?［J］. Clin Infect Dis, 2008, 46 (9): 1346-1352.
［9］Rubins JB, Duane PG, Clawson D, Charboneua D, Young J, Niewoehner DE. Toxicity of pneumolysin to pulmonary alveolar epithelial cells［J］. Infect Immun, 1993, 61(4): 1352-1358.
［11］Henrichsen J. Six newly recognized types of Streptococcus pneumoniae［J］. J Clin Microbiol, 1995, 33(10): 2759-2762.
［12］Hsieh YC, Tsao PN, Chen CL, Lin TL, Lee WS, Shao PL, et al. Establishment of a young mouse model and identification of an allelic variation of zmpB in complicated pneumonia caused by Streptococcus pneumoniae［J］. Crit Care med, 2008, 36(4): 1248-1255.
［15］Sorensen GL, Husby S, Holmskov U. Surfactant protein A and surfactant protein D variation in pulmonary disease［J］. Immunobiology, 2007, 212(4-5): 381-416.
［17］Fehrenbach H, Brasch F, Uhlig S, Weisser M, Stamme C, Wendel A, et al. Early alterations in intracellular and alveolar surfactant of the rat lung in response to endotoxin ［J］. Am J Respir Crit Care Med, 1998, 157 (5 Pt 1):1630-1639.
