AB0049 Eotaxin is overexpressed in churg-strauss syndrome compared to allergic asthma
Authors: M. Labrador-Horrillo, M. Ramentol, F. Martínez-Valle, R. Solans-Laqué, J. A. Bosch
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Historically, allergic asthma has been considered the background of the development of Churg-Strauss Syndrome (CSS)<sup>1,2</sup>. Recently, a retrospective study comparing CSS and allergic asthma proved that respiratory atopy or allergy, at least to known and currently tested allergens, are present in approximately only the 30% of CSS patients, compared to near the 60% in patients with allergic asthma<sup>3</sup>. In the last years, a new family of chemokines, named eotaxins, have increasingly been proved to be a powerful chemotactic agent for eosinophils, inducing the activation and the migration of eosinophil to the inflammation site<sup>4</sup>. Indeed, an increase in eotaxin levels (though locally or in peripheral blood) has been proved in several eosinophil-mediated diseases (including allergy and CSS)<sup>5</sup>. <h3>Objectives</h3> The aim of our study is to focus in the differences and similarities at the immunologic response level between CSS and allergic asthma. In this first part of a wider work, we studied the levels of eotaxin in peripheral blood samples from patients with CSS and allergic asthma. <h3>Methods</h3> We collected peripheral blood samples from patients with CSS in clinical remission and from a cohort of patients with allergic asthma most of whom presented signs and symptoms of mild to moderate disease activity. We determined the concentration of eotaxin using a cytometric bead array (CBA) assay from BD™ using a monoclonal antibody against human CC chemokine eotaxin. <h3>Results</h3> We compared eotaxin levels from 19 patients with CSS in clinical remission with a cohort of 9 patients with allergic asthma. Results were as follows: <h3>Conclusions</h3> Indeed, eotaxin play an important role in both diseases. Nonetheless, in CSS reaches higher levels, probably translating a prominent polarization of the T cell response towards a Th2 profile. Notably, despite lacking clinical evidence of CSS activity, eotaxin levels remain elevated, highlighting the presence of a treatment resistant immunological activity. <h3>References</h3> Solans R, Bosch JA, Perez-Bocanegra C, Selva A, Huguet P, Alijotas J, et al. Churg-Strauss syndrome: outcome and long-term follow-up of 32 patients. Rheumatology (Oxford) 2001;40(7):763-71 Guillevin L, Cohen P, Gayraud M, Lhote F, Jarrousse B, Casassus P. Churg-Strauss syndrome. Clinical study and long-term follow-up of 96 patients. Medicine (Baltimore) 1999;78(1):26-37 Bottero P, Bonini M, Vecchio F, Grittini A, Patruno GM, Colombo B, et al. The common allergens in the Churg-Strauss syndrome. Allergy 2007;62(11):1288-94 Conroy DM, Williams TJ. Eotaxin and the attraction of eosinophils to the asthmatic lung. Respir Res 2001;2(3):150-6 Polzer K, Karonitsch T, Neumann T, Eger G, Haberler C, Soleiman A, et al. Eotaxin-3 is involved in Churg-Strauss syndrome--a serum marker closely correlating with disease activity. Rheumatology (Oxford) 2008;47(6):804-8 <h3>Disclosure of Interest</h3> None Declared