Induction of GSNO reductase but not NOS in the lungs of mice exposed to glucan-spiked dust.

Both in vivo and in vitro studies have suggested that airborne organic dusts may induce inflammatory responses in the lungs, characterized by typical patterns of cytokine up-regulation and secretion. Recent work showed that exposure to glucan-spiked dust might influence nasal and pulmonary function, without an accompanying inflammatory response. However, effects of glucan-spiked dust exposure on NOS and GSNO reductase (enzymes important to NO signaling) remain less clear. This study aims to determine the effects of simultaneous exposure to glucan-spiked dust on NO signaling pathway in the airway. Danish Office dust was spiked with 1% (1-3)-ß-glucan (curdlan). Mice were exposed to 20 µL PBS (controls), 20 µL 25 µg/20 µL OVA and 20 µL 100 µg/20 µL glucan-spiked dust, respectively, daily for 12 days. NOS and GSNO reductase activity were measured in lung homogenate. Glutathione concentration and SOD activity in lung tissue were also determined to evaluate changes in oxidative stress. IL-6 concentration was measured in lungs to quantify the inflammatory response. Results showed that 12 day OVA and glucan-spiked dust exposure did not significantly influence NOS activity, GSH concentration, SOD activity, or IL-6 concentration. An insignificant increase in GSNOR activity and expression was observed in 12 day OVA-exposed mice, whereas glucan-spiked dust exposure significantly increased GSNOR activity and expression. Our results suggested that repeated glucan-spiked dust exposure to the airway could activate GSNO reductase but not NOS. Since GSNO reductase plays a pivotal role in NO signaling, these results may have clinical importance.