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Am J Physiol Lung Cell Mol Physiol (November 15, 2002). doi:10.1152/ajplung.00325.2002
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Articles in PresS, published online ahead of print November 15, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00325.2002
Submitted on September 26, 2002
Accepted on November 11, 2002

Surfactant strengthens the inhibitory effect of C-reactive protein on human lung macrophage-cytokine release

CRISTINA CASALS1*, JAVIER ARIAS-DIAZ2, FERNANDO VALINO1, ALEJANDRA SAENZ1, CRUZ GARCIA3, JOSE L. BALIBREA2, and ELENA VARA3

1 Department of Biochemistry and Molecular Biology I, Complutense University of Madrid, Madrid, Spain
2 Department of Surgery, San Carlos Hospital, Madrid, Spain
3 Department of Biochemistry and Molecular Biology III, Complutense University of Madrid, Madrid, Spain

* To whom correspondence should be addressed. E-mail: ccasalsc{at}bio.ucm.es.

In this study we investigated the effect of acute-phase levels of C-reactive protein (CRP) on cytokine production by pulmonary macrophages in the presence or absence of pulmonary surfactant. Both human alveolar and interstitial macrophages as well as human surfactant were obtained from multiple organ donor lungs. Precultured macrophages were stimulated with LPS alone or together with {gamma}IFN in the presence or absence of CRP, surfactant, and combinations. Releases of TNF{alpha} and of IL-1{beta} to the medium were determined. We found that CRP could modulate lung inflammation in humans by decreasing the production of proinflammatory cytokines by both alveolar and interstitial macrophages stimulated with LPS alone or together with {gamma}IFN. The potential interaction between CRP and surfactant phospholipids did not overcome the effect of either CRP or surfactant on TNF{alpha} and IL-1{beta} release by lung macrophages. On the contrary, CRP and pulmonary surfactant together had a greater inhibitory effect than either alone on the release of proinflammatory cytokines by lung macrophages.




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