HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Meloni, F. Articles by Baritussio, A. Search for Related Content PubMed PubMed Citation Articles by Meloni, F. Articles by Baritussio, A.

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.