Cigarette smoke extract enhances rhinovirus-induced toll-like receptor 3 expression and interleukin-8 secretion in A549 cells

2009 ◽  
Vol 23 (6) ◽  
pp. 5-9 ◽  
Author(s):  
Jong Hwan Wang ◽  
Hyuk Kim ◽  
Yong Ju Jang
Keyword(s):  
Cigarette Smoke ◽  
A549 Cells ◽  
Cigarette Smoke Extract ◽  
Interleukin 8 ◽  
Toll Like Receptor

Cytotoxic effects of cigarette smoke extract on an alveolar type II cell-derived cell line

2001 ◽  
Vol 281 (2) ◽  
pp. L509-L516 ◽  
Author(s):  
Yuma Hoshino ◽  
Tadashi Mio ◽  
Sonoko Nagai ◽  
Hiroyuki Miki ◽  
Isao Ito ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Cigarette Smoke ◽  
A549 Cells ◽  
Cigarette Smoke Extract ◽  
Alveolar Type ◽  
Type Ii ◽  
Cytotoxic Effects ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

Injury of the alveolar epithelium by cigarette smoke is presumed to be an important process in the pathogenesis of smoking-related pulmonary diseases. We investigated the cytotoxic effects of cigarette smoke extract (CSE) on an alveolar type II cell-derived cell line (A549). CSE caused apoptosis at concentrations of 5% or less and necrosis at 10% or more. When CSE was exposed to air before application to A549 cells, the cytotoxic effects were attenuated. CSE caused cell death without direct contact with the cells. Acrolein and hydrogen peroxide, two major volatile factors in cigarette smoke, caused cell death in a similar manner. Aldehyde dehydrogenase, a scavenger of aldehydes, and N-acetylcysteine, a scavenger of oxidants and aldehydes, completely inhibited CSE-induced apoptosis. CSE and acrolein increased intracellular oxidant activity. In conclusion, apoptosis of alveolar epithelial cells may be one of the mechanisms of lung injury induced by cigarette smoking. This cytotoxic effect might be due to an interaction between aldehydes and oxidants present in CSE or formed in CSE-exposed cells.

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