title: Eotaxin-3 is involved in Churg-Strauss syndrome--a serum marker closely correlating with disease activity.
abstract: OBJECTIVE
  Churg-Strauss Syndrome (CSS) is characterized by excessive eosinophil accumulation in peripheral blood and affected tissues with development of granulomatous vasculitic organ damage. The contribution of eosinophil-chemotactic cytokines (eotaxin family) to eosinophilia and disease activity in CSS is unknown. Thus, we compared serum levels of the eotaxin family members in CSS patients with healthy and disease controls.
  
  
  METHODS
  Forty patients with CSS diagnosed according to ACR 1990 criteria, 30 healthy controls (HC) and 57 disease controls (28 asthma, 20 small vessel vasculitis, 9 hypereosinophilic syndrome) were studied. Clinical data were collected and serum levels of eotaxin-1, -2 and -3 were determined by ELISA. Further, immunohistochemistry was applied to identify eotaxin-3 expression in tissue biopsies from patients with CSS.
  
  
  RESULTS
  In contrast to eotaxin-1 and -2, eotaxin-3 was highly elevated in serum samples of active CSS patients and correlated highly significantly with eosinophil counts, total immunoglobulin E (IgE) levels and acute-phase parameters. Moreover, eotaxin-3 was not elevated in other eosinophilic and vasculitic diseases. Immunohistochemical analysis revealed strong expression of eotaxin-3 in endothelial and inflammatory cells in affected tissues of active CSS patients.
  
  
  CONCLUSIONS
  This study reveals the specific association of elevated eotaxin-3 expression with high disease activity and eosinophilia in CSS patients. Eotaxin-3 might thus be a pathogenic player, biomarker and potential therapeutic target in CSS.
authors.affiliation: Department of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nuremberg, Krankenhausstrasse 12, 91054 Erlangen, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Polzer
authors.forename: T
authors.initials: T
authors.lastname: Karonitsch
authors.forename: T
authors.initials: T
authors.lastname: Neumann
authors.forename: G
authors.initials: G
authors.lastname: Eger
authors.forename: C
authors.initials: C
authors.lastname: Haberler
authors.forename: A
authors.initials: A
authors.lastname: Soleiman
authors.forename: B
authors.initials: B
authors.lastname: Hellmich
authors.forename: E
authors.initials: E
authors.lastname: Csernok
authors.forename: J
authors.initials: J
authors.lastname: Distler
authors.forename: B
authors.initials: B
authors.lastname: Manger
authors.forename: K
authors.initials: K
authors.lastname: Redlich
authors.forename: G
authors.initials: G
authors.lastname: Schett
authors.forename: J
authors.initials: J
authors.lastname: Zwerina
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D001706:Biopsy; D054413:Chemokine CCL11 / Q000097:blood; D054423:Chemokine CCL24 / Q000097:blood; D000075906:Chemokine CCL26; D019742:Chemokines, CC / Q000097:blood* / Q000378:metabolism; D015267:Churg-Strauss Syndrome / Q000097:blood* / Q000378:metabolism / Q000473:pathology; D004802:Eosinophilia / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D014657:Vasculitis / Q000097:blood
chemical_list: D015415:Biomarkers; C515456:CCL11 protein, human; C515484:CCL24 protein, human; C120429:CCL26 protein, human; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC