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Am J Physiol Lung Cell Mol Physiol 284: L360-L367, 2003. First published October 11, 2002; doi:10.1152/ajplung.00158.2002
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Vol. 284, Issue 2, L360-L367, February 2003

Decreased alveolar oxygen induces lung inflammation

C. Madjdpour1,2, U. R. Jewell1, S. Kneller1,2, U. Ziegler3, R. Schwendener4, C. Booy1, L. Kläusli3, T. Pasch2, R. C. Schimmer5, and B. Beck-Schimmer1,2

Institutes of 1 Physiology, 2 Anesthesiology, and 3 Anatomy, and 5 Department of Surgery, University of Zurich, 8057 Zurich; and 4 Paul Scherrer Institute, 5232 Villigen, Switzerland

Molecular mechanisms of the inflammatory reaction in hypoxia-induced lung injury are not well defined. Therefore, effects of alveolar hypoxia were studied in rat lungs, exposing rats to 10% oxygen over periods of 1, 2, 4, 6, and 8 h. An increase in the number of macrophages in bronchoalveolar lavage fluid of hypoxic animals was shown between 1 and 8 h. Extravasation of albumin was enhanced after 1 h and remained increased throughout the study period. NF-kappa B-binding activity as well as mRNA for TNF-alpha , macrophage inflammatory protein (MIP)-1beta , and monocyte chemoattractant protein (MCP)-1 were increased within the first 2 h of exposure to hypoxia. Hypoxia-inducible factor (HIF)-1alpha and intercellular adhesion molecule (ICAM)-1 mRNA were upregulated between 1 and 6 h. Elimination of alveolar macrophages by intratracheal application of liposome-encapsulated clodronate led to a decreased expression of NF-kappa B binding activity, HIF-1alpha , TNF-alpha , ICAM-1, and MIP-1beta . In summary, alveolar hypoxia induced macrophage recruitment, an increase in albumin leakage, and enhanced expression of inflammatory mediators, which were mainly macrophage dependent. Alveolar macrophages appear to have a prominent role in the inflammatory response in hypoxia-induced lung injury and the related upregulation of inflammatory mediators.

hypoxia; inflammatory mediators; lung injury


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