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Am J Physiol Lung Cell Mol Physiol 283: L94-L102, 2002. First published February 22, 2002; doi:10.1152/ajplung.00434.2001
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Vol. 283, Issue 1, L94-L102, July 2002

Combined SP-A-bleomycin effect on cytokines by THP-1 cells: impact of surfactant lipids on this effect

Weixiong Huang1, Guirong Wang1, David S. Phelps2, Hamid Al-Mondhiry3, and Joanna Floros1,2

Departments of 1 Cellular and Molecular Physiology, 2 Pediatrics, and 3 Medicine, Pennsylvania State College of Medicine, Hershey, Pennsylvania 17033

Surfactant protein A (SP-A) plays a role in host defense and inflammation in the lung. In the present study, we investigated the hypothesis that SP-A is involved in bleomycin-induced pulmonary fibrosis. We studied the effects of human SP-A on bleomycin-induced cytokine production and mRNA expression in THP-1 macrophage-like cells and obtained the following results. 1) Bleomycin-treated THP-1 cells increased tumor necrosis factor (TNF)-alpha , interleukin (IL)-8, and IL-1beta production in dose- and time-dependent patterns, as we have observed with SP-A. TNF-alpha levels were unaffected by treatment with cytosine arabinoside. 2) The combined bleomycin-SP-A effect on cytokine production is additive by RNase protection assay and synergistic by enzyme-linked immunosorbent assay. 3) Although the bleomycin effect on cytokine production was not significantly affected by the presence of surfactant lipid, the additive and synergistic effect of SP-A-bleomycin on cytokine production was significantly reduced. We speculate that the elevated cytokine levels resulting from the bleomycin-SP-A synergism are responsible for bleomycin-induced pulmonary fibrosis and that surfactant lipids can help ameliorate pulmonary complications observed during bleomycin chemotherapy.

chemotherapeutic agent; enzyme-linked immunosorbent assay; synergistic effect; ribonuclease protection assay; surfactant protein A


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