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Epithelial neutrophil-activating peptide-78 recruits neutrophils into pleural effusion

¹ Institute of Respiratory Diseases, First Affiliated Hospital, Guangxi Medical University, Nanning, Guangxi, and ² Dept of Respiratory Disease, Second Hospital of Medical School of Zhejiang University, Hangzhou, Zhejiang, China.

CORRESPONDENCE: H-Z. Shi, Institute of Respiratory Diseases, First Affiliated Hospital, Guangxi Medical University, Nanning 530021, Guangxi, China. E-mail: shihuanzhong{at}sina.com

Keywords: Infections, inflammatory cell, neutrophil migration, pleural effusion

Received: July 22, 2008
Accepted November 6, 2008

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 on 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.