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Am J Physiol Lung Cell Mol Physiol 294: L161-L174, 2008. First published November 30, 2007; doi:10.1152/ajplung.00169.2007
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INVITED REVIEW

INVITED REVIEW

Pathogenesis of the systemic inflammatory syndrome and acute lung injury: role of iron mobilization and decompartmentalization

Anna L. Lagan, Daniel D. Melley, Timothy W. Evans, and Gregory J. Quinlan

Department of Critical Care Medicine, Imperial College School of Medicine, Royal Brompton Hospital, London, United Kingdom

Changes in iron homeostatic responses routinely accompany infectious or proinflammatory insults. The systemic inflammatory response syndrome (SIRS) and the development of acute lung injury (ALI) feature pronounced systemic and lung-specific alterations in iron/heme mobilization and decompartmentalization; such responses may be of pathological significance for both the onset and progression of acute inflammation. The potential for excessive iron-catalyzed oxidative stress, altered proinflammatory redox signaling, and provision of iron as a microbial growth factor represent obvious adverse aspects of altered in vivo iron handling. The release of hemoglobin during hemolytic disease or surgical procedures such as those utilizing cardiopulmonary bypass procedures further impacts on iron mobilization, turnover, and storage with associated implications. Genetic predisposition may ultimately determine the extent to which SIRS and related syndromes develop in response to such changes. The design of specific therapeutic interventions based on endogenous stratagems to limit adverse aspects of altered iron handling may prove of therapeutic benefit for the treatment of SIRS and ALI.

systemic inflammatory response; hemolysis; oxidative stress


Address for reprint requests and other correspondence: G. J. Quinlan, Dept. of Critical Care Medicine, Royal Brompton Hospital, Sydney St., London SW3 6NP, UK (e-mail: g.quinlan{at}imperial.ac.uk)






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