1. ¹Department of Immunology, University of Connecticut Health Center, Farmington, CT, USA
2. ²Department of Pathology, University of Connecticut Health Center, Farmington, CT, USA
3. ³Department of Pediatrics, University of Connecticut Health Center, Farmington, CT, USA

Correspondence: Dr CM Schramm, Pulmonary Division, Connecticut Children's Medical Center, 282 Washington Street, Hartford, CT 06106, USA. E-mail: schramm@neuron.uchc.edu

Received 28 December 2007; Revised 22 March 2008; Accepted 26 March 2008; Published online 6 May 2008.

Abstract

Acute exposure of sensitized mice to antigen elicits allergic airway disease (AAD) characterized by Th2 cytokine-dependent pulmonary eosinophilia, methacholine hyperresponsiveness and antigen-specific IgE elevation. However, chronic exposure induces a local inhalational tolerance (LIT), with resolution of the airway responses but persistent systemic IgE production. To further determine if systemic immunologic responses were maintained during LIT, we assessed subcutaneous late phase responses to ovalbumin in this model. Sensitized and AAD mice developed small subcutaneous responses to ovalbumin, with footpad thickness increasing to 113.7 and 113.6% of baseline, respectively. In comparison, LIT mice developed marked foot swelling (141.6% ). Histologic examination confirmed increased inflammation in the chronic animals, with a significant contribution by eosinophils. Thus, the resolution of airway inflammatory responses with chronic antigen inhalation is a localized response, not associated with loss of systemic responses to antigen.