• M J Thomassen, L T Buhrow, and H P Wiedemann.
• Department of Pulmonary and Critical Care Medicine, The Cleveland Clinic Foundation, OH 44195-5038, USA.
• Crit. Care Med. 1997 Dec 1; 25 (12): 2045-7.

ObjectiveTo determine whether inflammatory cytokine production by stimulated human alveolar macrophages is affected by perflubron exposure.DesignControlled laboratory investigation of alveolar macrophage function in vitro.SettingResearch laboratory.SubjectsCultured alveolar macrophages obtained by bronchoalveolar lavage from eleven normal volunteers.InterventionsEndotoxin-stimulated alveolar macrophages were treated with perflubron.Measurements And Main ResultsAlveolar macrophages were stimulated for 1 hr with lipopolysaccharide and then treated with perflubron for 23 hrs. Cell-free supernatants were collected and cytokines were assayed by enzyme-linked immunosorbent assay. Tumor necrosis factor-alpha, interleukin-1, and interleukin-6 were stimulated by lipopolysaccharide (endotoxin) and all of these cytokines were significantly (p < .05) inhibited by perflubron. Cell viability was not affected by perflubron. Basal cytokine concentrations from unstimulated alveolar macrophages were not altered by perflubron.ConclusionsExposure of stimulated human alveolar macrophages to perflubron in vitro decreases cytokine production. This observation suggests that perflubron may have anti-inflammatory activity.

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