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Table 1 Cigarette smoke extract did not cause proinflammatory cytokine (IL-8 and IL-6) release in transformed alveolar epithelial cells

From: Differential effects of cigarette smoke on oxidative stress and proinflammatory cytokine release in primary human airway epithelial cells and in a variety of 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***

  1. 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.