Application of liquid, aerosolized, and vaporized perfluorocarbons (PFC) in acute lung injury has shown anti-inflammatory effects. Although this may be beneficial in states of pulmonary hyperinflammation, it also could increase susceptibility to nosocomial lung infection. We hypothesized that PFC impair cellular host defense and therefore investigated in an in vitro model the influence of perfluorohexane (PFH) on crucial mechanisms of bacterial elimination in human neutrophils and monocytes. Using scanning and transmission electron microscopy, we could show membrane-bound and ingested PFH particles that morphologically did not alter adherence and phagocytosis of Escherichia coli or leukocyte viability. The amount of adherent and phagocytosed bacteria as determined by flow cytometry was not influenced in cells only pretreated with PFH for 1 and 4 h. When PFH was present during E. coli challenge, bacterial adherence was decreased in polymorphonuclear neutrophils, but respective intracellular uptake was not impaired and was even significantly promoted in monocytes. Overall, E. coli-induced respiratory burst capacity was not reduced by PFH. Our findings provide evidence that key functions of innate host defense are not compromised by PFH treatment in vitro.phagocytosis; burst; perfluorohexane; anti-inflammatory; immune LIQUID VENTILATION WITH PERFLUOROCARBONS (PFC) has been successfully applied in experimental and human acute lung injury (18,20,27,36). Beside positive effects on gas exchange, lung mechanics, and ventilation/perfusion matching, animals treated with liquid ventilation also exhibited attenuated pulmonary damage with concomitant reduction in pulmonary neutrophil sequestration (19,21,32,39). A clinical trial investigating PFC treatment in trauma patients with acute lung injury demonstrated reduced neutrophil counts and decreased levels of proinflammatory cytokines in bronchoalveolar lavage fluid (7). Although removal of alveolar inflammatory exudate by dense, water-insoluble PFC probably contributes to mitigation of pulmonary hyperinflammation, a direct interference with immune cell function may also be involved. This proposition is supported by recent in vivo studies using aerosolized PFC in a surfactant-washout model that reported PFC to decrease mRNA expression of proinflammatory cytokines and adhesion molecules in lung tissue samples as well as in microdissected alveolar macrophages and pulmonary parenchymal cells (42,49,50). Further evidence for cellular anti-inflammatory effects of PFC is provided by in vitro experiments showing a decreased response of activated polymorphonuclear neutrophils (PMN) and monocytic cells in terms of cytokine secretion, chemotaxis, cyclooxygenase-2 (COX-2) expression, and NF-B activation (5,25,37,46,51). Liquid ventilation with PFC did not result in improved survival or reduced need for ventilatory support in recent multicenter trials of patients with acute respiratory distress syndrome (ARDS) (17, 24). Nevertheless, intrinsic anti-inflammatory properties of PFC might b...

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