Acute nitrogen dioxide (NO2) exposure enhances airway inflammation via modulating Th1/Th2 differentiation and activating JAK-STAT pathway

Abstract

Nitrogen dioxide (NO2) is an air pollutant associated with poor respiratory health, asthma exacerbation, and an increased likelihood of inhalational allergies. However, the underlying mechanisms are not clear. In the present study, the airway inflammatory response was first assessed in rats exposed to 5mg/m(3) NO2 for seven days. The results showed that NO2 exposure caused the pulmonary pathological alteration, and significantly stimulated MUC5AC expression. Following this, obviously up-regulated changes of pro-inflammatory cytokines (IL-1β, IL-6, and ICAM-1) were observed. Also, NO2 inhalation induced the imbalance in the ratio of Th1/Th2 differentiation (IL-4, IFN-γ, GATA-3 and T-bet) and the activation of following JAK-STAT pathway (JAK1, JAK3 and STAT6). The findings clarify an important mechanism for NO2 inhalation being injurious to the lung and augmenting the degree of allergic airway inflammation.

Keywords: Airway inflammation; JAK-STAT pathway; NO(2); Th1/Th2 differentiation.