PT  - JOURNAL ARTICLE
AU  - F. Meloni
AU  - A. Alberti
AU  - A. Bulgheroni
AU  - A. Lupi
AU  - E. Paschetto
AU  - A. Marone Bianco
AU  - G. Rodi
AU  - A. Fietta
AU  - M. Luisetti
AU  - A. Baritussio
TI  - Surfactant apoprotein A modulates interleukin-8 and monocyte chemotactic peptide-1 production
AID  - 10.1183/09031936.02.00211102
DP  - 2002 Jun 01
TA  - European Respiratory Journal
PG  - 1128--1135
VI  - 19
IP  - 6
4099  - http://erj.ersjournals.com/content/19/6/1128.short
4100  - http://erj.ersjournals.com/content/19/6/1128.full
SO  - Eur Respir J2002 Jun 01; 19
AB  - Previous studies have shown that surfactant apoprotein A (SP-A) and natural or synthetic surfactant can modulate the release of pro-inflammatory cytokines from alveolar mononuclear phagocytes. The aim of this study was to assess whether SP-A or Surfactant (Surf) from patients with pulmonary alveolar proteinosis (PAP) can affect the release of two chemokines (interleukin (IL)-8 and monocyte chemtactic peptide (MCP)-1) from human monocytes and rat lung type-II cells. In addition IL-8 and MCP-1 levels were assessed in the brochoalveolar lavage fluid (BALF) of seven patients with PAP and compared with those in a group of control subjects (n=5). SP-A, tested over a wide range of concentrations, significantly increased IL-8 and MCP-1 release from monocytes. SP-A retained its activity after collagenase digestion, but was not active after heat treatment. The release of IL-8 by monocytes was also stimulated by Surf. Finally, median BALF IL-8 and MCP-1 levels in PAP patients were significantly higher than in controls (9.50 and 9.51 pg·mL−1 in controls versus 151.95 and 563.70 pg·mL−1 in PAP, respectively) and significantly correlated with SP-A concentrations in BALF. Overall the results of this study support the view that the high content of alveolar surfactant apoprotein A may contribute to the upregulation of chemokine release in pulmonary alveolar proteinosis, thus contributing to airway inflammation.