title: Eotaxin-1, -2, and -3 immunoreactivity and protein concentration in the nasal polyps of eosinophilic chronic rhinosinusitis patients.
abstract: OBJECTIVE
  Eosinophilic chronic rhinosinusitis (CRS) is characterized by the accumulation of numerous eosinophils in the sinus mucosa and nasal polyps, which are frequently difficult to control, even with surgery. The present study was designed to evaluate the expression and localization of eotaxins, which are well known to be potent and selective chemoattractants for eosinophils in CRS.
  
  
  METHODS
  Randomized study.
  
  
  METHODS
  The patients were classified into eosinophilic and noneosinophilic groups. Histopathological profiles of the nasal polyp were observed with hematoxylin-eosin staining. Eotaxin-1, -2, and -3 were immunohistochemically stained in the nasal polyps. Furthermore, the protein content of eotaxin subtypes inside the nasal polyp and sinus effusion was measured using enzyme-linked immunosorbent assay (ELISA).
  
  
  RESULTS
  In the nasal polyps, immunoreactivities of the eotaxin subfamily, eotaxin-1, -2, and -3, were noted in most of the infiltrating eosinophils, as well as in other inflammatory cells, epithelial cells, and endothelial cells. Compared with noneosinophilic CRS groups, eosinophilic CRS groups had a significant expression of eotaxins in their eosinophils. The eotaxin concentrations of nasal polyp and sinus effusion as measured by ELISA were significantly increased in the eosinophilic CRS group compared to the noneosinophilic CRS group.
  
  
  CONCLUSIONS
  The present findings suggest that enhanced eotaxin family production by eosinophils results in the recruitment of eosinophils into the tissue by a self-amplifying process. Laryngoscope, 2009.
authors.affiliation: Department of Otorhinolaryngology, and BioMedical Research Center, Juntendo University School of Medicine, Tokyo, Japan.
authors.forename: Toru
authors.initials: T
authors.lastname: Yao
authors.forename: Yuko
authors.initials: Y
authors.lastname: Kojima
authors.forename: Akemi
authors.initials: A
authors.lastname: Koyanagi
authors.forename: Hidenori
authors.initials: H
authors.lastname: Yokoi
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Saito
authors.forename: Kenji
authors.initials: K
authors.lastname: Kawano
authors.forename: Masayuki
authors.initials: M
authors.lastname: Furukawa
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kusunoki
authors.forename: Katsuhisa
authors.initials: K
authors.lastname: Ikeda
mesh_terms: D000328:Adult; D000368:Aged; D001249:Asthma / Q000473:pathology; D054413:Chemokine CCL11 / Q000032:analysis*; D054423:Chemokine CCL24 / Q000032:analysis*; D000075906:Chemokine CCL26; D019742:Chemokines, CC / Q000032:analysis*; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000473:pathology*; D004804:Eosinophils / Q000473:pathology; D005260:Female; D006801:Humans; D007958:Leukocyte Count; D008297:Male; D015523:Maxillary Sinusitis / Q000473:pathology*; D008875:Middle Aged; D009092:Mucous Membrane / Q000473:pathology; D009297:Nasal Mucosa / Q000473:pathology; D009298:Nasal Polyps / Q000473:pathology*; D010256:Paranasal Sinuses / Q000473:pathology; D012221:Rhinitis, Allergic, Perennial / Q000473:pathology*
chemical_list: C120429:CCL26 protein, human; D054413:Chemokine CCL11; D054423:Chemokine CCL24; D000075906:Chemokine CCL26; D019742:Chemokines, CC