title: Pleural fluid levels of vascular cell adhesion molecule-1 are elevated in eosinophilic pleural effusions.
abstract: OBJECTIVE
  The mechanisms responsible for the accumulation of eosinophils in pleural fluid are not fully understood. The objective of the present study was to examine the relationship between pleural fluid eosinophilia and the levels of vascular cell adhesion molecule (VCAM)-1, eotaxin, RANTES (regulated upon activation, normal T-cell expressed and secreted), and interleukin (IL)-4 in pleural effusions.
  
  
  METHODS
  Thirty-one patients with eosinophilic pleural effusion (EPE) [eosinophil percentage > 10% of the pleural fluid nucleated cells] and 10 patients without EPE were evaluated. VCAM-1, eotaxin, RANTES, and IL-4 in all pleural fluids were measured using enzyme-linked immunosorbent assay kits. IL-5 levels of the same fluids were measured in a previous study.
  
  
  RESULTS
  VCAM-1, eotaxin, and RANTES but not IL-4 were detectable in the pleural fluids. The mean level of VCAM-1 in EPE (336 +/- 85 ng/mL) was significantly higher (p = 0.011) than that in the noneosinophilic effusions (260 +/- 34 ng/mL) [mean +/- SD]. VCAM-1 levels were significantly correlated with the eosinophil count and percentage in all pleural fluids (r = 0.43, p = 0.005, and r = 0.37, p = 0.019, respectively). Multiple linear regression analysis disclosed that both IL-5 (beta, 0.63; p < 0.001) and VCAM-1 (beta, 0.27, p = 0.025) are independent predictors of the number of eosinophils in all pleural fluids. RANTES and eotaxin did not differ significantly between EPEs and non-EPEs, and were not correlated with the number of pleural fluid eosinophils.
  
  
  CONCLUSIONS
  The levels of VCAM-1 are increased in EPE, suggesting that VCAM-1 is important in the pathogenesis of EPE. Neither eotaxin nor RANTES is associated with pleural fluid eosinophilia.
authors.affiliation: Department of Critical Care and Pulmonary Services, Athens Medical School, Evangelismos Hospital, Athens, Greece.
authors.forename: Ioannis
authors.initials: I
authors.lastname: Kalomenidis
authors.forename: Kamel H
authors.initials: KH
authors.lastname: Mohamed
authors.forename: Kirk B
authors.initials: KB
authors.lastname: Lane
authors.forename: R Stokes
authors.initials: RS
authors.lastname: Peebles
authors.forename: Randal
authors.initials: R
authors.lastname: Barnette
authors.forename: R Michael
authors.initials: RM
authors.lastname: Rodriguez
authors.forename: Richard W
authors.initials: RW
authors.lastname: Light
mesh_terms: D054413:Chemokine CCL11; D018946:Chemokine CCL5 / Q000032:analysis; D019742:Chemokines, CC / Q000032:analysis; D002631:Chemotactic Factors, Eosinophil / Q000032:analysis; D004797:Enzyme-Linked Immunosorbent Assay; D004802:Eosinophilia / Q000378:metabolism*; D006801:Humans; D015847:Interleukin-4 / Q000032:analysis; D015848:Interleukin-5 / Q000032:analysis; D016014:Linear Models; D010996:Pleural Effusion / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000032:analysis*
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D018946:Chemokine CCL5; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D015848:Interleukin-5; D019010:Vascular Cell Adhesion Molecule-1; D015847:Interleukin-4