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

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.