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Cigarette smoke extract did not cause proinflammatory cytokine (IL-8 and IL-6) release in transformed alveolar epithelial cells |
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| Cell line |
Treatment |
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| Control |
CSE (1.0%) |
CSE (2.5%) |
CSE (5.0%) |
TNF-α (10 ng/ml) |
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| Interleukin-8 (IL-8) pg/ml |
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| Human lung cancer cells (H1299) |
51.3 ± 3.2 |
53.7 ± 4.7 |
56.5 ± 7.4 |
45.1 ± 3.1 |
432 ± 59.1*** |
| Human adenocarcinoma cells (A549) |
623 ± 52.9 |
635 ± 52.4 |
620 ± 80.1 |
612 ± 76.3 |
1200 ± 100*** |
| Human papillary adenocarcinoma cells (H441) |
200 ± 27.2 |
210 ± 35.1 |
200 ± 58.4 |
198 ± 39.2 |
384 ± 28.1*** |
| Interleukin-6 (IL-6) pg/ml |
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| Rat lung epithelial cells (L2) |
40.2 ± 4.8 |
43.1 ± 5.2 |
41.5 ± 7.2 |
38.8 ± 2.6 |
165 ± 14.5*** |
| Murine type II epithelial cells (MLE-15) |
35.6 ± 2.3 |
31.4 ± 5.5 |
38.1 ± 2.3 |
31.9 ± 3.6 |
74.5 ± 5.7*** |
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Alveolar epithelial cell lines (H1299, A549, H441, L2 and MLE-15) were treated for 24 hr with cigarette smoke extract (1.0–5.0%) prepared from 1R3F research grade cigarettes and TNF-α was used as a positive control (10 ng/ml). Cells were harvested, and supernatants were collected for the measurement of IL-8 and IL-6 levels by sandwich ELISA. Cigarette smoke extract treatment did not show any significant change in IL-8 and IL-6 release in any of the transformed cell lines, whereas TNF-α treatment induced proinflammatory cytokine (IL-8 and IL-6) release. Data represent mean ± SEM of 3 individual experiments. ***p < 0.001 compared to control values. CSE: cigarette smoke extract. | |||||
Kode et al. Respiratory Research 2006 7:132 doi:10.1186/1465-9921-7-132 |
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