Role of heme oxygenase in pulmonary response to antigen challenge in sensitized rats in vivo

Heme oxygenase (HO) protects against oxidant-mediated lung injury. However, it is uncertain whether changes in HO activity modulate antigen-induced airway inflammation. We studied the effects of pretreatment with either hemoglobin, a HO inducer, or tin protoporphyrin (SnPP)-9, a specific HO inhibitor, on increases in pulmonary insufflation pressure (PIP) and plasma extravasation induced by intravenously injected ovalbumin (OA) antigen in rats sensitized to OA in vivo with Evans blue dye as a marker. Pretreatment with hemoglobin (300 mg/kg) significantly increased (p < 0.01) and that with SnPP-9 (50 μmol/kg) significantly decreased (p < 0.01) HO activity of the lung, but they failed to alter OA antigen (300 μg/kg)-induced increases in PIP. In contrast, hemoglobin pretreatment significantly decreased (p < 0.01) and SnPP-9 pretreatment significantly increased (p < 0.05) the leakage of dye induced by OA antigen in the trachea, main bronchi, and segmental bronchi. OA antigen-induced increases in plasma extravasation were also inhibited by superoxide dismutase (12,000 U/kg). These findings suggest the oxygen radicals are involved in increases in plasma extravasation induced by antigen challenge and HO protects against antigen-induced airway inflammation.