title: Eotaxin-2 and eotaxin-3 expression is associated with persistent eosinophilic bronchial inflammation in patients with asthma after allergen challenge.
abstract: BACKGROUND
  Eotaxin-1, eotaxin-2, and eotaxin-3 are chemokines involved in the activation and recruitment of eosinophils through activation of their main receptor, CC chemokine receptor 3. The differential roles of these chemokines still remain to be established. It has been suggested that eotaxin-1 is an important mediator in the early phase of allergen-induced recruitment of eosinophils into the airways. Eotaxin-2 and eotaxin-3 might play a role in the subsequent persistence of allergen-induced bronchial eosinophilia.
  
  
  OBJECTIVE
  The aim of this study was to determine the expression of eotaxins and eosinophil counts in the bronchial mucosa of subjects with mild asthma after resolution of the late-phase asthmatic response (LAR).
  
  
  METHODS
  The expression of eotaxins and eosinophil counts were determined in bronchial biopsy specimens obtained from 10 subjects with mild asthma 48 hours after diluent and allergen challenge by using immunohistochemistry. Positively stained cells were counted in a 125-mum-deep zone of the lamina propria.
  
  
  RESULTS
  Eotaxin-2 and eotaxin-3 expression in bronchial mucosa was significantly increased 48 hours after allergen challenge ( P = .001 and P = .013, respectively). At this time point, when marked tissue eosinophilia was still present, these increases were positively correlated with the magnitude of the LAR ( r = 0.72, P = .019 and r = 0.64, P = .046, respectively). Furthermore, eotaxin-2 expression was associated with the number of eosinophils after allergen challenge ( r = 0.72, P = .018).
  
  
  CONCLUSIONS
  Our findings suggest that eotaxin-2 and eotaxin-3 might account for the persistence of bronchial eosinophilia after resolution of the LAR.
authors.affiliation: Department of Pulmonology, Lung Function Laboratory C2-P-62, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands. A.J.J.Ravensberg@lumc.nl
authors.forename: A Janneke
authors.initials: AJ
authors.lastname: Ravensberg
authors.forename: Fabio L M
authors.initials: FL
authors.lastname: Ricciardolo
authors.forename: Annemarie
authors.initials: A
authors.lastname: van Schadewijk
authors.forename: Klaus F
authors.initials: KF
authors.lastname: Rabe
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Sterk
authors.forename: Pieter S
authors.initials: PS
authors.lastname: Hiemstra
authors.forename: Thais
authors.initials: T
authors.lastname: Mauad
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D015214:Antigens, Differentiation, Myelomonocytic / Q000378:metabolism; D001249:Asthma / Q000276:immunology / Q000378:metabolism*; D001980:Bronchi / Q000276:immunology / Q000378:metabolism; D001985:Bronchial Provocation Tests; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC / Q000096:biosynthesis*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology* / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000378:metabolism; D008297:Male; D008407:Mast Cells / Q000276:immunology / Q000378:metabolism; D011657:Pulmonary Eosinophilia / Q000276:immunology*; D020545:Respiratory Mucosa / Q000378:metabolism; D000097382:CD68 Molecule
chemical_list: D015703:Antigens, CD; D015214:Antigens, Differentiation, Myelomonocytic; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC; C515484:CCL24 protein, human; C120429:CCL26 protein, human; C067980:CD68 antigen, human; D000097382:CD68 Molecule