The aim of this study was to investigate the presence of epithelial neutrophil-activating peptide (ENA)-78 in pleural effusions, as well as the chemoattractant activity of pleural ENA-78 0n neutrophils. Pleural effusion and serum samples were collected from 75 patients who presented to the respiratory institute (19 with malignant pleural effusion, 21 with tuberculous pleural effusion, 18 with infectious pleural effusion and 17 with transudative pleural effusion). The concentrations of ENA-78, myeloperoxidase and neutrophil elastase were determined, and the chemoattractant activity of ENA-78 for neutrophils both in vitro and in vivo was also observed. The concentrations of ENA-78, myeloperoxidase and neutrophil elastase in infectious pleural effusion were significantly higher than those in malignant, tuberculous and transudative groups, respectively (all p<0.01). Infectious pleural fluid was chemotactic for neutrophils in vitro and anti-ENA-78 antibody could partly inhibit these chemotactic effects. Intrapleural administration of ENA-78 produced a marked progressive influx of neutrophils into pleural space. Compared with noninfectious pleural effusion, ENA-78 appeared to be increased in infectious pleural effusion. Our data suggested that ENA-78 was able to induce neutrophil infiltration into pleural space and might be responsible for pleural neutrophil degranulation.

The aim of the present study was to investigate effects of allergen inhalation and oral glucocorticoid on concentration of serum soluble CD86 in patients with allergic asthma. Our results showed that the serum soluble CD86 concentrations in the dual responder group increased from 491.8 F 15.4 IU/ml before allergen inhalation to 603.8 F 19.3 IU/ml 24 h after allergen inhalation. In the isolated early responders, there was no significant increase in serum soluble CD86 concentrations after allergen inhalation compared with baseline levels. There was a significant decrease in serum soluble CD86 concentrations after 2 weeks of glucocorticoid therapy (448.3 F 15.1 IU/ml) compared with baseline values (532.7 F 12.3 IU/ml), whereas there was no significant difference in the placebo group. This study has demonstrated that serum soluble CD86 concentrations increased after allergen inhalation in sensitized asthmatic subjects, and that serum sCD86 concentrations were downregulated by prednisolone therapy.