Journal of Pathology and Translational Medicine

Original Articles

Apoptosis of Alveolar Cells in Pneumocystis Carinii Pneumonia: Application of Electron Microscopic Terminal Deoxynucleotidyl Transferase-Mediated dUTP-Biotin Nick End Labeling Method.: Kyu Hun Kang, Sang Pyo Kim, Kun Young Kwon; Korean J Pathol. 2001;35(6):496-505.

Abstract: BACKGROUND
Pneumocystis carinii (P. carinii) attaches to alveolar cells and causes injury to the epithelial cells by direct toxic effects or inhibition of epithelial growth and replication. Although respiratory cell damage or death is a common feature in P. carinii pneumonia, there has been little reports about expression of apoptosis of the lung tissue in the literatures.
METHODS
We examined expression of fibronectin and vitronectin in the interaction between P. carinii and alveolar cells, and in situ terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end-labeling (TUNEL) expression of apoptosis in the respiratory cells by immunohistochemistry and pre-embedding immunoelectron microscopy.
RESULTS
Light microscopic (LM) and electron microscopic (EM) immunohistochemical stains for the fibronectin and vitronectin showed strong expressions on the pellicles and tubular extensions of P. carinii and weak expression along the surfaces of type I alveolar cells. LM and EM TUNEL stains showed positive expression in the nuclei of alveolar cells, apoptotic bodies in the cytoplasm of alveolar macrophages and cellular debris in alveolar spaces.
CONCLUSIONS
P. carinii induces injury and apoptosis of alveolar cells after attachment of the organisms to host cells, and alveolar macrophages enhance the clearance of apoptotic bodies of alveolar cells as well as phagocytosis and degradation of P. carinii.

The Pattern of Cell Proliferation and Apoptosis in Human Embryonic and Fetal Brain.: Suk Jin Choi, Jung Ran Kim; Korean J Pathol. 2002;36(1):38-44.

Abstract PDF: BACKGROUND
Cell proliferation and apoptosis account for the major morphogenetic mechanisms during development of the central nervous system. We investigated these processes in developing human brains.
METHODS
We examined human embryonic and fetal brains. Cell proliferation was analysed by classical histology and MIB-1 immunohistochemistry; cell death was investigated by the TdT-mediated dUTP-biotin nick end labelling method.
RESULTS
Most proliferating cells were observed in the ventricular zone (VZ) in the 3rd-10th week of gestational age (GA), and in both the VZ and the subventricular zone (SV) in the 19-24th week of GA. The proliferation index of the VZ was highest in the 8th week of GA and then decreased as the GA advanced. Apoptotic cells were observed in the VZ as early as the 5th week of GA. They were also observed in the intermediate zone in the 19-24th week of GA, although they were significantly lower in amount compared to that in the VZ and SV.
CONCLUSIONS
These results suggest that apoptosis occurring early in the embryonic period is related to a cellular mechanism which selects and determines the cells that are committed to migration and differentiation during the development of the human brain.

Reducing Effect of Angiotensin-1 Converting Enzyme Inhibitor (Captopril) in Fibrosis of Radiation Induced Lung Injury.: Kun Young Kwon, Hae Ra Jung, Sun Young Kwon, Jin Hee Kim, Ok Bae Kim; Korean J Pathol. 2004;38(3):145-156.

Abstract PDF: BACKGROUND
The captopril reduces radiation induced lung injury and fibrosis. We designed a study to evaluate the antifibrogenic effect of Captopril in radiation induced lung injury.
METHODS
Fifty Sprague-Dawley rats were divided into radiation group (I) (n=30) and radiation plus captopril group (II) (n=15). The rats were sacrificed at 12 hours and 11 weeks after radiation. We examined light microscopic, immunohistochemical and electron microscopic features in each groups.
RESULTS
In Group I, the lungs showed acute lung injury at 12 h. The lungs showed patchy fibrosis with collagen deposits at 11 weeks. The severity of the alveolar injury and fibrosis was correlated with radiation doses. The Group II showed less severe lung fibrosis than Group I. The mean numbers of mast cells and myofibroblasts of Group II were lower than Group I (p< 0.05). The TNF-alpha and TGF-beta were higher expressed according to radiation doses in Group I, and less prominent in Group II. Ultrastructurally, the alveolar cell injury and fibrosis were less severe in Group II. The TUNEL stains showed higher expressions according to radiation doses in Group I, and expressed in Group II.
CONCLUSIONS
The captopril decreases the number of mast cells and myofibroblasts, reduces collagen deposition and apoptosis of alveolar cells in rat lungs after radiation, and so reduces the degree of pulmonary injury and fibrosis.

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