BACKGROUND: Tobacco cigarette smoke (TCS) was previously demonstrated to affect the innate and adaptive immune responses as a consequence of oxidant generation which play a pivotal role in neutrophilic airway inflammation. Aim of this paper was to investigate whether electronic cigarette smoke (ECS) generates reactive oxygen species (ROS) similarly to cigarette smoke. METHOD: By means of a house made apparatus, ECS and TCS were collected in fetal bovine serum (FBS) which was used to grow immune cells isolated from rats. As index of oxidative products nitrite, superoxide, and thiobarbituric acid-reactive substances (TBARS) were determined in the medium before and after cell growth. RESULTS: The results showed that: i) ECS caused a remarkable increase of nitrites and TBARS although in lesser extension than TCS; ii) the spleen and lymph node cells grown in ECS and TCS-exposed medium were able to reduce TBARS but not nitrites present in the medium; iii) PBMC in TCS-exposed medium were able to reduce nitrites and TBARS more efficiently than spleen and lymph node cells, but released more superoxide anion; iv) TCS and ECS not influence the PBMC and spleen T cell subtype populations (CD4+, CD8+). CONCLUSIONS: As ECS nicotine-free gave the same results of unexposed medium, we can support the hypothesis that the increase of ROS in ECS exposed medium was prevalently due to nicotine.
ASJC Scopus subject areas
- Public Health, Environmental and Occupational Health