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B activation and lung
injury induced by hepatic ischemia-reperfusion
Department of Surgery, University of Louisville School of Medicine, Louisville, Kentucky 40292
Hepatic
ischemia and reperfusion cause local and remote organ injury.
This injury culminates from an integrated cascade of proinflammatory
cytokines, chemokines, and adhesion molecules, many of which are
regulated by the transcription factor nuclear factor-
B (NF-B).
The anti-inflammatory cytokine interleukin-10 (IL-10) has been shown to
have inhibitory effects on NF-B. The objective of the current study
was to determine whether IL-10 could suppress pulmonary NF-B
activation and ensuing lung injury induced by hepatic
ischemia-reperfusion. C57BL/6 mice underwent partial hepatic
ischemia with or without intravenous administration of IL-10.
Hepatic ischemia-reperfusion resulted in pulmonary NF-B activation, increased mRNA expression of tumor necrosis factor-
(TNF-), and macrophage inflammatory protein-2 (MIP-2), as well as
increased pulmonary neutrophil accumulation and lung edema. Administration of IL-10 suppressed lung NF-B activation, reduced TNF- and MIP-2 mRNA expression, and decreased pulmonary neutrophil recruitment and lung injury. The data suggest that IL-10 protects against hepatic ischemia and reperfusion-induced lung injury by inhibiting lung NF-B activation and the resulting pulmonary
production of proinflammatory mediators.
inflammation; tumor necrosis factor-; neutrophils; mice; nuclear
factor-B
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