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- Evaluation of Bronchiolar and Alveolar Cell Injuries Induced by Short- and Long-term Exposure to Sidestream Smoke
- Kun-Young Kwon, Hye-Ra Jung, Ilseon Hwang, Won-Il Choi
- Korean J Pathol. 2012;46(2):151-161. Published online April 25, 2012
- DOI: https://doi.org/10.4132/KoreanJPathol.2012.46.2.151
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Abstract
PDF Background We investigated effects of short- and long-term exposure to sidestream smoke on the bronchiolar and alveolar cells in Sprague-Dawley rats.
Methods Rats were divided into five experimental groups: groups 1, 2, and 3 (1-month exposure to 3, 5, and 7 cigarettes a day, respectively), groups 4 and 5 (3- and 6 month exposure to five cigarettes a day, respectively). We examined the morphologic changes, the expressions of tumor necrosis factor α (TNF-α), tumor growth factor β1 (TGF-β1), interlekin (IL)-1α, IL-1β, Ki-67, and cytokeratin 14 and
in situ apoptosis in the bronchiolar and alveolar cells on light microscopy (LM) and electron microscopic (EM) terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining.Results LM showed the respiratory bronchiolar dilatation and alveolar wall collapse. In groups 3, 4, and 5, EM showed loss of the cilia and Clara cells with irregular size, more prominent alveolar wall collapse and dilation of alveolar duct than those of groups 1 and 2. Bronchiolar and alveolar cells showed increased expressions of TNF-α and TGF-β in groups 4 and 5. LM and EM TUNEL stains showed increased apoptosis in groups 3, 4, and 5.
Conclusions Sidestream smoke causes a bronchiolar and alveolar cell injury and the severity correlates strongly the volume and duration of exposure to sidestream smoke.
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Citations
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- Cigarette smoke extract alters the cell cycle via the phospholipid transfer protein/transforming growth factor-β1/CyclinD1/CDK4 pathway
Xue-Min Chai, You-Lun Li, Hong Chen, Shu-Liang Guo, Li-Li Shui, Ya-Juan Chen
European Journal of Pharmacology.2016; 786: 85. CrossRef - Keratin-14 Expression in Pneumocytes as a Marker of Lung Regeneration/Repair during Diffuse Alveolar Damage
Miriam Ficial, Caterina Antonaglia, Marco Chilosi, Mario Santagiuliana, Al-Omoush Tahseen, Davide Confalonieri, Lorenzo Zandonà, Rossana Bussani, Marco Confalonieri
American Journal of Respiratory and Critical Care Medicine.2014; 189(9): 1142. CrossRef
- Cigarette smoke extract alters the cell cycle via the phospholipid transfer protein/transforming growth factor-β1/CyclinD1/CDK4 pathway
- Morphologic Changes of Pulmonary Tissue Secondary to Sidestream Cigarette Smoke.
- Kun Young Kwon, Ji Min Jeon, Sang Pyo Kim, Kwan Kyu Park, Dae Hyun Kim
- Korean J Pathol. 1999;33(6):395-403.
- 1,460 View
- 15 Download
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Abstract
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- Chronic bronchiolitis is a condition associated with cigarette smoking, and later associated with pulmonary parenchymal alteration and progressive deterioration of lung function. Early respiratory bronchiolitis was produced in Sprague-Dawley rats by indirect inhalation of cigarette smoke daily in a smoke exposure chamber designed by authors for 1 month. Experimental group A (n=5) was sacrificed after having smoked 30 cigarettes, group B (n=5) after 80 cigarette, and group C (n=7) after 140 cigarettes, respectively. Examination of morphologic changes in the lungs was done on light microscope, transmission and scanning electron microscopes. Light microscopically, increase in number of goblet cells in the bronchial mucosa, brown-pigmented macrophages in the alveoli, multifocal alveolar collapse adjacent to the bronchioles, dilatation of alveolar ducts and alveolar spaces were observed. Transmission electron microscopically, irregularly shaped Clara cells, alveolar wall collapse, and focally type I epithelial cell injury were seen. Scanning electron microscopically, scattered alveolar collapse, irregular dilatation of alveolar ducts, alveolar spaces and interalveolar pores (pores of Kohn) were seen. The terminal and respiratory bronchioles showed morphological alteration of Clara cells, but no evidence of cellular bronchiolitis or bronchiolar obstruction. We conclude that sidestream smoke induces an early respiratory bronchiolitis including aggregates of brown pigmented macrophages and varying degrees of structural alteration of adjacent pulmonary parenchyma.
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