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AB0049 Eotaxin is overexpressed in churg-strauss syndrome compared to allergic asthma
  1. M. Labrador-Horrillo1,
  2. M. Ramentol2,
  3. F. Martínez-Valle2,
  4. R. Solans-Laqué2,
  5. J. A. Bosch2
  1. 1Allergic Diseases
  2. 2Internal Medicine, Hospital Vall d’Hebron, Barcelona, Spain

Abstract

Background Historically, allergic asthma has been considered the background of the development of Churg-Strauss Syndrome (CSS)1,2. 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 asthma3. 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 site4. Indeed, an increase in eotaxin levels (though locally or in peripheral blood) has been proved in several eosinophil-mediated diseases (including allergy and CSS)5.

Objectives 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.

Methods 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.

Results 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:

Conclusions 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.

  1. 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

  2. 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

  3. 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

  4. Conroy DM, Williams TJ. Eotaxin and the attraction of eosinophils to the asthmatic lung. Respir Res 2001;2(3):150-6

  5. 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

Disclosure of Interest None Declared

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