Cigarette smoke-induced NF-kappaB activation in human lymphocytes: the effect of low and high exposure to gas phase of cigarette smoke.

Cigarette smoking is linked to various human disorders. Active and passive smokers suffer from inflammatory diseases of lungs and airways. Smoking-dependent airway inflammation is related to the cytotoxic effects of cigarette smoke (CS) and chronic recruitment of neutrophils and macrophages. NF-kappaB is a key inflammatory, redox-sensitive transcription factor. Its role in CS-induced airway inflammation is unclear. This study investigated CS-induced NF-kappaB activation in human lymphocytes and the possible involvement of oxidative insult in this activation. A method for accurate and reproducible exposure of lymphocytes to CS was developed. The intensity of CS exposure was linearly correlated with nitrite concentration originating from reactive oxygen species in CS. Mild, but not high exposure to CS, induced NF-kappaB in lymphocytes through the increase in oxidative stress and the reduction in the intracellular glutathione levels. These findings may have implications to active as well as to passive smokers, suffering from inflammatory diseases of lungs and airways.