Epinephrine promotes pulmonary angiitis: evidence for a β1-adrenoreceptor-mediated mechanism

Abstract

Epinephrine (Epi) increases lymphocyte traffic to lung. We investigated whether Epi also modulates pulmonary cell-mediated immune responses in vivo. C57BL/6 mice were immunized with hen-egg lysozyme (HEL) on day 0, challenged with HEL intratracheally at day 12, and killed at day 15. Mice received Epi (0.5 mg/kg) subcutaneously during the sensitization phase, days 1–7 (Epi-SP), or the effector phase, days 12–14 (Epi-EP); controls received saline subcutaneously. Epi-SP mice showed increased airway inflammation ( P < 0.03) and pulmonary angiitis ( P < 0.04) characterized by endothelialitis and subendothelial fibrin deposition. Macrophages and granulocytes were increased in perivascular cuffs in situ ( P < 0.001). CD3+ lymphocytes increased in the bronchoalveolar lavage fluid, whereas NK1.1+ and CD4+CD25+ lymphocytes decreased (all P < 0.05). Atenolol, a selective β1-adrenoreceptor (AR) antagonist, inhibited the increased vascular and airway inflammation and the reduction in CD4+CD25+ lymphocytes (all P < 0.05) yielded by Epi, whereas all α/β-AR blockers inhibited airway inflammation. We conclude that Epi-EP selectively promotes vascular inflammation in vivo via a β1-receptor-mediated mechanism.