Background: Cigarette smoke exposure (CSE) results in extensive inflammation in the upper and lower airways. Reactive oxygen species, such as superoxide, have been shown to be potent mediators of this inflammation.
Methods: Mucosal biopsy specimens were collected from patients undergoing sinonasal surgery and were used as a source of primary epithelial cells. Human sinonasal epithelial (HSNE) cells and were isolated from sinus tissue, maintained in culture, and ultimately treated with varying concentrations of CSE with or without free superoxide dismutase (SOD). Supernatants and cell lysates were examined for the proinflammatory cytokine interleukin (IL)-8. Similar experiments were performed using normal human bronchial epithelial (NHBE) cell lines.
Results: CSE induces both secretion and intracellular production of the proinflammatory cytokine IL-8 by HSNE cells in a dose-dependent manner. Furthermore, this up-regulation can be suppressed by SOD. CSE induces secretion of IL-8 in NHBEs that is also suppressed by SOD.
Conclusion: Inflammation in the airway after CSE can be blocked by SOD in this in vitro model. The ability to attenuate CSE-induced inflammation with SOD could provide a therapeutic/preventative approach for individuals with cigarette smoke exposure.