RT Journal Article
SR Electronic
T1 Surfactant apoprotein A modulates interleukin-8 and monocyte chemotactic peptide-1 production
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 1128
OP 1135
DO 10.1183/09031936.02.00211102
VO 19
IS 6
A1 F. Meloni
A1 A. Alberti
A1 A. Bulgheroni
A1 A. Lupi
A1 E. Paschetto
A1 A. Marone Bianco
A1 G. Rodi
A1 A. Fietta
A1 M. Luisetti
A1 A. Baritussio
YR 2002
UL http://erj.ersjournals.com/content/19/6/1128.abstract
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.