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Mechanisms of Lung Epithelial Cell Injury by Pseudomonas Aeruginosa

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Molecular Biology of Acute Lung Injury

Abstract

The interactions between hosts and pathogens have evolved to select for gene combinations that can confer an advantage to either combatant. Bacteria have evolved several methods of inducing cell injury and are an important cause of acute lung injury (ALI). This review focuses on Pseudomonas aeruginosa, a soil bacterium that expresses many toxins that damage epithelial cells and can cause significant lung injury in critically ill patients (1). P. aeruginosa is rapidly becoming an important model system to better understand bacterial-host interactions leading to ALI. The recent sequencing and annotation of the P. aeruginosa genome will allow for microarray analyses to test the relevance of bacterial gene expression relative to host responses in several kinds of animal models. Moreover, the Pseudomonas research community already has a wealth of fundamental information regarding virulence gene and protein expression, and the delivery of toxic substances and enzymes to their cellular targets. Many laboratories are moving rapidly toward a phase where the individual virulence attributes, their expression, function, and regulation will be integrated into the biology of this metabolically and genetically versatile organism.

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Wiener-Kronish, J.P., Frank, D., Sawa, T. (2001). Mechanisms of Lung Epithelial Cell Injury by Pseudomonas Aeruginosa . In: Wong, H.R., Shanley, T.P. (eds) Molecular Biology of Acute Lung Injury. Molecular and Cellular Biology of Critical Care Medicine, vol 1. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1427-5_10

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  • DOI: https://doi.org/10.1007/978-1-4615-1427-5_10

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