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Part of the book series: Update in Intensive Care and Emergency Medicine ((UICMSOFT,volume 44))

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Conclusion

Sepsis is increasing in incidence and is commonly complicated by organ failure, of which the lung is the most common. Pronounced changes in cellular iron regulation occur in such patients, leading to dysregulation of the inflammatory response through the regulation of pro-oxidant potential and apoptotic function. The availability of heme substrate determines the nature of a range of responses to pro-inflammatory stimuli, especially in endothelial cells and neutrophils. HO-1 expression accompanies these changes and early indications suggest that fluxes in cellular iron levels direct the responses. Clinically relevant mechanical and biological stimuli result in similar pro-inflammatory responses in alveolar epithelial (like) cells, suggesting that a common signaling pathway directs iron-mediated responses. Finally, damage to alveolar epithelial cell and the microvascular endothelium leads to changes in pulmonary structure and function that characterize ALI/ARDS.

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MacCallum, N.S., Quinlan, G.J., Evans, T.W. (2007). Pulmonary Dysfunction. In: Abraham, E., Singer, M. (eds) Mechanisms of Sepsis-Induced Organ Dysfunction and Recovery. Update in Intensive Care and Emergency Medicine, vol 44. Springer, Berlin, Heidelberg . https://doi.org/10.1007/3-540-30328-6_25

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