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1Department for Neonatology and Pediatric Intensive Care Medicine, Klinik für Kinderheilkunde, Universitätsklinikum Carl Gustav Carus, Medizinische Fakultät der Technischen Universität Dresden, Dresden; 2Clinic for Neonatology, Charité Universitätsmedizin Berlin, Campus Virchow-Klinikum, and 3Clinic for Neonatology, Charité Universitätsmedizin Berlin, Campus Mitte, Berlin, Germany
Submitted 30 March 2007 ; accepted in final form 4 March 2008
Perfluorocarbons (PFC) reduce the production of various inflammatory cytokines, including TNF-
. The anti-inflammatory effect is not entirely understood. If anti-inflammatory properties are caused by a mechanical barrier, PFC in the alveoli should have no effect on the inflammatory response to intravenous LPS administration. To test that hypothesis, rats (n = 31) were administered LPS intravenously and were either spontaneously breathing (Spont), conventionally ventilated (CMV), or receiving partial liquid ventilation (PLV). Serum concentration of TNF-
was measured. The pulmonary expressions of TNF-
and TNF-
receptor 1 protein and of TNF-
and ICAM-1 mRNA were determined. LPS caused a significant (P < 0.001) increase in serum TNF-
. Serum TNF-
concentration was similar in LPS/Spont (525 ± 180 pg/ml) and LPS/CMV (504 ± 154 pg/ml) but was significantly (P < 0.001) lower in animals of the LPS/PLV group (274 ± 101 pg/ml). Immunohistochemical data on TNF-
protein expression showed a LPS-induced increase in TNF-
and TNF-
receptor 1 expression that was diminished by partial liquid ventilation. PCR measurements revealed a lower expression of TNF-
and ICAM-1 mRNA in LPS/PLV than in LPS/CMV or LPS/Spont animals. Semiquantitative histological evaluation revealed only minor alveolar inflammation with no significant differences between the groups. Low serum TNF-
concentration in PFC-treated animals is most likely explained by a decreased production of TNF-
in the lung.
fluorocarbons; tumor necrosis factor-
; lipopolysaccharide; liquid ventilation; anti-inflammatory agents
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