Source: Annual Congress 2002 - Cellular reactions in allergy in humans and animals
Disease area: Airway diseases

Abstract

Many features of bronchial asthma such as smooth muscle contraction, mucus secretion and infiltration of inflammatory cells are consistent with the action of anaphylotoxins, C3a and C5a. Data from animal and human studies suggest the involvement of these anaphylotoxins in allergic asthma. A recombinant soluble form of the mouse membrane complement inhibitor Crry-Ig demonstrates decay-accelerating activity for both the classical and alternative pathways of complement. To delineate the role of the complement system in the development of AHR and lung eosinophilia, we studied the effects of Crry-Ig in a model of allergic airway inflammation. Crry-Ig was administered to sensitized mice by intraperitoneal injection or by aerosol 2 h before three airway allergic challenges and 36 h before assay. Airway function was monitored by changes in lung resistance (RL) and dynamic compliance (Cdyn) to inhaled methacholine (MCh). After OVA sensitization and airway challenge of C57BL/6 mice, AHR was increased as did the number of lung inflammatory cells when compared to non-sensitized animals. Sensitized and challenged mice developed increased serum levels of OVA-specific IgE and IgG1 with a significant airway eosinophilia and heightened responsiveness to MCh. Administration of Crry-Ig significantly prevented both development of AHR as well as BALF eosinophilia compared with untreated mice. Crry-Ig treatment decreased OVA specific IgG1. Treatment with Crry-Ig also resulted in a significant increase in IL-12 production in BALF. These results indicate that Crry-Ig may have a therapeutic role in the treatment of allergic airway inflammation and asthma.

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Y. H. Rha, C. Taube, A. Joetham, A. Dakhama, M. V. Holers, E. W. Gelfand (Denver, United States Of America; Seoul, South Korea). Role of complement receptor-related gene y (Crry)-Ig in allergic airway inflammation and hyperresponsiveness. Eur Respir J 2002; 20: Suppl. 38, 299

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