Interaction of tobacco smoke exposure and ovalbumin-sensitization promotes goblet cell and submucosal gland metaplasia in guinea pigs

- The long term impact of tobacco smoke exposure and airway antigen sensitization on the number of mucous secreting cells is investigated.
- Inflammatory responses to prolonged tobacco smoke exposure and airway sensitization are enhanced compared to 3 other experimental groups including airway reactivity to ovalbumin, goblet cells, submucosal cells and eosinophilia.
- Variables of tobacco smoke exposure or antigen sensitization alone which induce little airway inflammation when combined induce enhanced including airway reactivity to ovalbumin and airway remodeling.

Exposure to irritants such as tobacco smoke (TS) causes acute airway inflammation. Chronic exposure may cause airway remodeling contributing to enhanced airway resistance. We hypothesize that combining airway sensitization and inhalation of irritants enhances the number of mucous producing cells beyond either agent alone. Guinea pigs were antigen sensitized or treated with its vehicle. These two groups were further divided into daily exposure to TS or air. After 3 months airway reactivity to ovalbumin (OA) was determined, airway and blood samples were examined and lung substance P quantified. Combining sensitization and TS exposure increased airway reactivity to OA, goblet cell and submucosal gland populations. Airway eosinophilia was greatest in the OA-sensitized group exposed to air rather than with its combination with TS exposure. Lung substance P levels were similarly elevated in both OA-sensitized groups. Airway irritant exposure in which airway sensitization exists enhances the potential of mucus production, airway resistance and mucus plugging of the airways through increasing the number of goblet cells and submucosal glands.