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Am J Physiol Lung Cell Mol Physiol 285: L232-L239, 2003. First published May 2, 2003; doi:10.1152/ajplung.00248.2002
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Epinephrine promotes pulmonary angiitis: evidence for a {beta}1-adrenoreceptor-mediated mechanism

Felipe A. Jain1, Long-hai Zhao1, Martin K. Selig1, and Richard L. Kradin1, 2

Immunopathology and Pulmonary and Critical Care Units, Massachusetts General Hospital, Boston, Massachusetts 02114

Submitted 26 July 2002 ; accepted in final form 6 March 2003

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 {beta}1-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 {alpha}/{beta}-AR blockers inhibited airway inflammation. We conclude that Epi-EP selectively promotes vascular inflammation in vivo via a {beta}1-receptor-mediated mechanism.

lung; vessels; airways; immunity; lymphocytes


Address for reprint requests and other correspondence: R. Kradin, Warren-5, Massachusetts General Hospital, Boston, MA 02114 (E-mail rkradin{at}partners.org).






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