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Am J Physiol Lung Cell Mol Physiol 284: L466-L472, 2003. First published November 15, 2002; doi:10.1152/ajplung.00325.2002
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Vol. 284, Issue 3, L466-L472, March 2003

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

Cristina Casals1, Javier Arias-Díaz2, Fernando Valiño1, Alejandra Sáenz1, Cruz García3, José L. Balibrea2, and Elena Vara3

Departments of Biochemistry and Molecular Biology 1 I and 3 III, and 2 Department of Surgery, San Carlos Hospital, Complutense University of Madrid, 28040 Madrid, Spain

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 IFN-gamma in the presence or absence of CRP, surfactant, and combinations. Releases of TNF-alpha and of IL-1beta 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 IFN-gamma . The potential interaction between CRP and surfactant phospholipids did not overcome the effect of either CRP or surfactant on TNF-alpha and IL-1beta 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.

human lung surfactant; interstitial macrophages; alveolar macrophages; lipopolysaccharide


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