Perfluorochemical liquids modulate cell-mediated inflammatory responses

To examine whether chemically different perfluorochemical liquids (PFC) (perfluorodecalin [PFD]; perflubron [PFB]) induce inflammatory responses in blood leukocytes.

University research laboratory.

Whole blood from 12 healthy adults was incubated with increasing PFC concentrations and/or bacterial lipopolysaccharide.

Adhesion molecules (CD62L, CD11b), reactive oxygen species, and cytokine responses in resting and activated leukocyte subtypes were studied. Scanning and transmission electron microscopies were performed. At the highest concentrations, PFB stimulated a significant increase in resting monocytic reactive oxygen species production; all types of blood leukocytes were unresponsive to PFD. Neither PFB nor PFD changed CD62L expression; PFB increased CD11b expression in monocytes and granulocytes. PFD induced a small though significant increase in interleukin-8 secretion. When simulating a condition in which patients with severe lung disease or sepsis would be ventilated with PFC, neither PFB nor PFD plus lipopolysaccharide stimulated tumor necrosis-alpha or interleukin-8 production above levels induced by lipopolysaccharide alone, but rather demonstrated a trend for decreased tumor necrosis factor-alpha production. Expression of CD11b and CD62L and the production of reactive oxygen species were not changed beyond the levels induced by lipopolysaccharide alone. As a morphologic correlate to the above proinflammatory changes, surface-bound blebs and intracellular vacuoles were seen by electron microscopy.

At PFC concentrations comparable with those in blood during liquid ventilation, PFC liquids did not induce variables associated with inflammation. In the presence of high PFC concentrations, simulating the condition in which bronchoalveolar cells are exposed to PFC, monocytes may be induced by PFB to produce reactive oxygen species, and blood leukocytes induced by PFB to express CD11b and by PFD to secrete interleukin-8; the presence of either PFC attenuated tumor necrosis factor-alpha production after lipopolysaccharide stimulation.