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Articles in PresS, published online ahead of print February 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00434.2001
Submitted on November 7, 2001
Accepted on February 12, 2002
1 Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, PA, USA
2 Pediatrics, Penn State College of Medicine, Hershey, PA, USA
3 Medicine, Penn State College of Medicine, Hershey, PA, USA
4 Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, PA, USA; Pediatrics, Penn State College of Medicine, Hershey, PA, USA
* To whom correspondence should be addressed. E-mail: jfloros{at}psu.edu.
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 TNF-
, IL-8, and IL-1ß production in dose and time-dependent patterns as we have observed with SP-A. TNF- levels were unaffected by treatment with cytosine arabinoside. 2) The combined bleomycin/SP-A effect on cytokine production is additive by ribonuclease protection assay and synergistic by ELISA. 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.
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