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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.