title: Eotaxin levels in pleural effusions: comparison with monocyte chemoattractant protein-1 and IL-8.
abstract: OBJECTIVE
  In order to investigate the role of eotaxin in pleural diseases, we measured eotaxin in pleural effusions and studied the relationship between eotaxin levels and recruitment of inflammatory cells, particularly eosinophils. Interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) levels were also measured for comparison.
  
  
  METHODS
  We evaluated 47 pleural effusion samples, 7 transudates and 40 exudates. The exudates consisted of 19 malignant, 11 tuberculous, and 5 parapneumonic effusions, and 5 effusions of other etiologies. Chemokine levels were measured by specific sandwich enzyme-linked immunosorbent assays.
  
  
  RESULTS
  Eotaxin was detected in all samples examined, but the levels did not differ significantly among the exudates. There was no significant correlation between the levels of eotaxin and MCP-1 or IL-8. The level of eotaxin but not the others was significantly higher in eosinophilic effusions (>10% eosinophils among white blood cells in the fluid) than in non-eosinophilic fluids. The number of eosinophils in pleural effusions was significantly correlated with the eotaxin levels, but not with the levels of other chemokines. The number of neutrophils was significantly correlated with IL-8 but not with the others.
  
  
  CONCLUSIONS
  Results suggest that eotaxin contributes to the migration of eosinophils in pleural inflammation. Taken together with the correlation between IL-8 and neutrophils, it appears that the predominant type of pleural inflammatory infiltrate is controlled, at least in part, by the subgroup of chemokines expressed in the pleural space.
authors.affiliation: Second Department of Internal Medicine, Ehime University School of Medicine, Shigenobu.
authors.forename: A
authors.initials: A
authors.lastname: Yokoyama
authors.forename: N
authors.initials: N
authors.lastname: Kohno
authors.forename: M
authors.initials: M
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Abe
authors.forename: K
authors.initials: K
authors.lastname: Hiwada
authors.forename: H
authors.initials: H
authors.lastname: Yamada
authors.forename: K
authors.initials: K
authors.lastname: Matsushima
authors.forename: K
authors.initials: K
authors.lastname: Hirai
mesh_terms: D054413:Chemokine CCL11; D018932:Chemokine CCL2 / Q000032:analysis*; D018925:Chemokines / Q000032:analysis; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil / Q000032:analysis*; D016207:Cytokines / Q000032:analysis*; D004804:Eosinophils / Q000502:physiology*; D006801:Humans; D016209:Interleukin-8 / Q000032:analysis*; D009000:Monocytes / Q000502:physiology; D010995:Pleural Diseases / Q000473:pathology; D010996:Pleural Effusion / Q000737:chemistry* / Q000503:physiopathology
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D018932:Chemokine CCL2; D018925:Chemokines; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D016207:Cytokines; D016209:Interleukin-8