The exposure of airway epithelium to virus, allergens, cigarette smoke and pollution can induce TSLP release, an alarmin that acts as an upstream activator of T2-high responses and that is involved in the promotion of remodeling processes.

The aim of this study was to investigate the relationship between oxidative stress and TSLP release at the level of the airway epithelium. We exposed to cigarette smoke extracts (CSE) a bronchial epithelial cell line (16HBE) and primary bronchial epithelial cells (PBEC) cultured at the air-liquid interface (ALI) and differentiated to form a pseudostratified epithelium. Intracellular and extracellular  oxidative stress was evaluated by flow cytometry and by an innovative electrochemical sensor, respectively. TSLP release was assessed by ELISA. TSLP concentrations in sera from non-smoker and smoker subjects were also evaluated.

The obtained results showed that, in 16HBE as well as in differentiated PBEC exposed to CSE, there is an increase in oxidative stress and this is associated to increased TSLP release. Accordingly, TSLP concentrations were significantly higher in sera from smokers than in sera from non-smokers.

In conclusion, data herein provided demonstrated that TSLP release and oxidative stress can be considered events strictly related to the injury promoted by cigarette smoke exposure in the airway epithelium. The detection of oxidative stress by electrochemical sensors can open new avenues for evaluating epithelial damage and to identify patients eligible to alarmin targeted biologics.