title: Recruitment of inflammatory cells to the pleural space. Chemotactic cytokines, IL-8, and monocyte chemotactic peptide-1 in human pleural fluids.
abstract: Pleural effusions secondary to various diseases are associated with the presence of different inflammatory cells. The role of selective chemotactic cytokines in the recruitment of phagocytes to the pleural space is unclear. IL-8 and monocyte chemotactic peptide-1 (MCP-1) are recently described cytokines that are chemotactic for neutrophils and monocytes, respectively. We prospectively studied 63 patients, using strictly defined criteria for their selection. IL-8 concentrations were elevated in both empyema fluid (9.15 +/- 0.89 ng/ml) and parapneumonic effusions (4.7 +/- 0.697 ng/ml) when compared with pleural effusions secondary to other diseases. IL-8 levels were higher in empyema fluid than in parapneumonic effusions (p = 0.01). There was a significant correlation between IL-8 levels and the total numbers of neutrophils in empyema fluids (r = 0.80). Chemotactic activity for neutrophils was elevated in empyema fluid and the addition of IL-8 neutralizing serum decreased bioactivity by 32.22%. Malignant pleural effusions had the highest levels of MCP-1 (12.0 +/- 3.7 ng/ml) when compared with others. Cytology-positive pleural fluids (n = 10) had a higher level of MCP-1 than cytology-negative effusions (p = < 0.05). Malignant pleural fluid MCP-1 levels correlated (r = 0.70) with the absolute number of monocytes in the pleural fluid. Neutralization of monocyte chemotactic activity of malignant pleural fluid by specific neutralizing serum caused a 70.3% inhibition of bioactivity. Immunohistochemical staining of malignant pleural fluid localized antigenic MCP-1 to malignant cells. We conclude that both IL-8 and MCP-1 play major but not exclusive roles in the recruitment of neutrophils and monocytes from the vascular compartment to the pleural space.
authors.affiliation: Department of Pulmonary and Critical Care Medicine, Veterans Administration Medical Center, Indianapolis, Indiana.
authors.forename: V B
authors.initials: VB
authors.lastname: Antony
authors.forename: S W
authors.initials: SW
authors.lastname: Godbey
authors.forename: S L
authors.initials: SL
authors.lastname: Kunkel
authors.forename: J W
authors.initials: JW
authors.lastname: Hott
authors.forename: D L
authors.initials: DL
authors.lastname: Hartman
authors.forename: M D
authors.initials: MD
authors.lastname: Burdick
authors.forename: R M
authors.initials: RM
authors.lastname: Strieter
mesh_terms: D018932:Chemokine CCL2; D002630:Chemotactic Factors / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism*; D004653:Empyema / Q000276:immunology / Q000473:pathology; D006333:Heart Failure / Q000276:immunology / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D016209:Interleukin-8 / Q000378:metabolism*; D010996:Pleural Effusion / Q000276:immunology* / Q000473:pathology*; D016066:Pleural Effusion, Malignant / Q000276:immunology / Q000473:pathology; D010998:Pleurisy / Q000209:etiology / Q000276:immunology / Q000473:pathology; D011014:Pneumonia / Q000276:immunology / Q000473:pathology; D014397:Tuberculosis, Pulmonary / Q000276:immunology / Q000473:pathology
chemical_list: D018932:Chemokine CCL2; D002630:Chemotactic Factors; D016207:Cytokines; D016209:Interleukin-8