Submitted on July 26, 2002
Accepted on March 6, 2003
Epinephrine Promotes Pulmonary Angiitis: Evidence for a B1-Adrenoreceptor Mediated Mechanism
Felipe A. Jain1, Long-hai Zhao1, Martin K. Selig1, and Richard L. Kradin2*
1 Department of Immunopathology, Massachusetts General Hospital, Boston, MA, USA
2 Department of Immunopathology, Massachusetts General Hospital, Boston, MA, USA; Department of Pulmonary and Critical Care Unit, Massachusetts General Hospital, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: rkradin{at}partners.org.
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 i.t. at day 12 and sacrificed at day 15. Mice received EPI (0.5mg/kg) s.q. during the sensitization phase at days 1-7 (EPI-SP) or the effector phase at days 12-14 (EPI-EP); controls received saline (SAL) s.q. 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 (ATEN), a selective 
1-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 
/-AR blockers inhibited airway inflammation. We conclude that EPI-EP selectively promotes vascular inflammation in vivo via a 1 receptor-mediated mechanism.
