E-submission
Search
- Page Path
- HOME > Search
- 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
- 7,561 View
- 38 Download
- 2 Crossref
-
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.
-
Citations
Citations to this article as recorded by
- 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
- The Role of MIB-1 Expression and Apoptosis in Experimental Crescentic Glomerulonephritis.
- Nam Hoon Kim, Wan Seop Kim, Jung Woo Noh, Moon Hyang Park
- Korean J Pathol. 1999;33(4):231-242.
- 1,662 View
- 14 Download
-
Abstract
PDF
- It has been postulated that programmed cell death via apoptosis may be critical for remodelling of glomeruli after inflammatory injury. To understand the regulatory mechanism of apoptosis in experimental crescentic glomerulonephritis (CGN), we examined the MIB-1 score (proliferation index, PI) and apoptotic index during the progression of experimental CGN to end-stage renal failure. CGN was induced in New Zealand White rabbits by administration of guinea pig anti-GBM IgG after sensitization with guinea pig IgG and their kidneys were analyzed for the development of crescents through sequential renal biopsies. Serum creatinine levels progressively increased in a time course until day 45. The PI in glomeruli, tubular epithelial cells, and interstitium progressively increased during the progression of experimental CGN. The mean numbers of MIB-1 positive intraglomerular nuclei (PI) were significantly correlated with degrees of crescent formation and the numbers of apoptotic cells in the glomeruli, tubules, and interstitium. Significant apoptosis was present from day 1 (15.8 10.16 cells/glomerular cross section) and increased in number with the proliferative lesions as glomerular inflammation continued. Moreover, apoptosis increased during the resolution of the glomerular inflammation, and many apoptotic cells were present in the sclerotic lesions in day 17 (18.6 12.99 cells/glomerular cross section). As glomerular inflammation subsided, cellular crescents progressed to fibrous crescents with a reduction of cellularity by day 45. On day 45, the glomerular PI and the numbers of apoptotic cells were markedly decreased. The correlations found in CGN between the creatinine level and the percentage of crescents, between the percentage of crescent and PI, and between the PI and number of apoptotic cells support the hypothesis that there is a change in the glomerular and tubulo-interstitial apoptosis under pathologic conditions. These findings indicate that apoptosis plays an essential role in the resolution of intra- and extraglomerular inflammation and in the elimination of glomerular cells within the sclerotic regions for progressive CGN. The regulation of the apoptotic phenomenon and increased PI during CGN may be important in the progression of glomerular inflammation and the development of pathologic glomerular sclerosis.
First
Prev
