Cigarette smoke is composed of more than 4000 compounds including 20 pulmonary carcinogens. It is well known that cigarette smoke contributes to the development of lung cancer, but there is limited information about its role in the formation and the proliferation of tumoral cells. Alveolar macrophages (AM) play a major role in pulmonary homeostasis via mediator production and cytotoxicity against tumoral cells. Therefore, we hypothesized that cigarette smoke extract (CSE) inhibits AM functions contributing to the development and the proliferation of tumoral cells.
NR8383, a rat AM cell line, was exposed or not to CSE 3% for 20 h in presence of LPS (10 ng/ml) and tumor necrosis factor (TNF) production was assessed in cell-free supernatants. AM cytotoxicity against WEHI-164, a TNF-sensitive fibrosarcoma cell line, was also measured using a chromium51 release assay.
CSE significantly inhibited both AM TNF production (41.53 ± 3.8 %) and TNF-dependent cytotoxicity (42.81 ± 1.08 % for control cells compared to 36.41 ± 1.40 % for exposed cells).
The inhibition of AM TNF production by CSE may contribute to the inhibition of AM cytotoxicity against TNF-sensitive cells.
A reduce cytotoxic activity of AM against tumoral cells may explain the persistence and the proliferation of these cells in people exposed to cigarette smoke.
Lea-Isabelle Proulx, None.