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Surfactant apoprotein A modulates interleukin-8 and monocyte chemotactic peptide-1 production

¹ Dept of Haematological, Pneumological and Cardiovascular Sciences, Respiratory Diseases Section and Clinic of Respiratory Diseases, University of Pavia and Istituto di Ricovero e Cura a Carattere Scientifico Policlinico San Matteo, Pavia, ² Institute of Internal Medicine, University of Padova, Padova and ³ First Intensive Care Unit, and Istituto di Ricovero e Cura a Carattere Scientifico Policlinico San Matteo, Pavia, Italy

CORRESPONDENCE: F. Meloni, Dipartimento di Scienze Ematologiche, Pneumologiche e Cardiovascolari mediche e chirurgiche, Sezione di Pneumologia, Universita di Pavia, I.R.C.C.S. Policlinico San Matteo, Padiglione Forlanini, Via Taramelli 5, 27100, Pavia, Italy. Fax: 39 0382422267. E-mail: federica-meloni@libero.it

Keywords: chemokines, interleukin-8, monocyte chemotactic peptide-1, pulmonary alveolar proteinosis, surfactant, surfactant apoprotein-A

Received: February 2, 2001
Accepted December 13, 2001

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.

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