Table 1

Cigarette smoke extract did not cause proinflammatory cytokine (IL-8 and IL-6) release in transformed alveolar epithelial cells

Cell line
Treatment



Control
CSE (1.0%)
CSE (2.5%)
CSE (5.0%)
TNF-α (10 ng/ml)


Interleukin-8 (IL-8) pg/ml
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
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***

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