Chronic exposure to sulfur dioxide enhances airway hyperresponsiveness only in ovalbumin-sensitized rats

Sulfur dioxide (SO2) is a common air pollutant that triggers asthmatic symptoms, but its toxicological mechanisms are not fully understood. Specifically, it is unclear how airborne SO2 affects airway hyperresponsiveness (AHR) – a hallmark feature of asthma. To this end, we investigated the effects of chronic exposure to SO2 on AHR, airway inflammation, tissue remodeling, cell stiffness (G′) and contractility of the airway smooth muscle cell (ASMC). Newborn Sprague–Dawley (SD) rats sensitized to ovalbumin (OVA) was used as the model to mimic asthmatic symptoms. The experimental results show that exposure to SO2: (1) significantly increased Penh (an indicator of AHR) in the OVA-sensitized rats (p < 0.01) but not in the normal rats (p > 0.05), which correlated with the increase of airway smooth muscle mass; (2) increased IL-4 production in BALF of both the normal (p < 0.05) and OVA-sensitized rats (p < 0.001), but decreased IFN-γ in BALF of only the normal rats, and in serum only increased IL-4 production of the OVA-sensitized rats (p < 0.001); (3) increased ASMC stiffness (G′) and contractility only in the OVA-sensitized rats (p < 0.001, p < 0.05, respectively). Taken together, these results demonstrate that SO2 may be a universal airway inflammatory factor, but more importantly, specific to exacerbating AHR in asthmatics only. These findings uncover a potential mechanism of SO2-induced health effects and may provide a basis for therapeutic targets.

► SD rats, either OVA-sensitized or not, were exposed to sulfur dioxide (SO2).
► The rats were examined for changes in structure and function of the airways.
► SO2 promoted airway inflammation in both OVA-sensitized and normal rats.
► SO2 enhanced airway hyperresponsiveness in OVA-sensitized, but not normal rats.
► SO2 may be a specific risk factor to worsen airway function of the asthmatics.