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Pseudomonas aeruginosa strains with lipopolysaccharide defects exhibit reduced intracellular viability after invasion of corneal epithelial cells.

作者信息

Evans David, Kuo Tracy, Kwong Mary, Van Rajana, Fleiszig Suzanne

机构信息

Morton D. Sarver Laboratory for Cornea and Contact Lens Research, School of Optometry, University of California at Berkeley, Berkeley, CA 94720, USA.

出版信息

Exp Eye Res. 2002 Dec;75(6):635-43. doi: 10.1006/exer.2002.2072.

DOI:10.1006/exer.2002.2072
PMID:12470965
Abstract

Pseudomonas aeruginosa is a leading cause of infectious keratitis. Many ocular isolates of this bacterium invade corneal epithelial cells in vitro and in vivo. Antibiotic survival assays have shown that a complete core lipopolysaccharide is required for full epithelial invasion by P. aeruginosa. In this study, we show that P. aeruginosa mutants with defects in their lipopolysaccharide core and O antigen exhibited reduced viability after internalization by corneal epithelial cells. Restoration of lipopolysaccharide core and O antigen expression by complementation with the plasmid pLPS1 restored intracellular survival. P. aeruginosa strains with a complete lipopolysaccharide survived and replicated within the cells. The data suggest that lipopolysaccharide is involved in the intracellular survival and/or replication of P. aeruginosa, indicating an additional mechanism by which this important virulence factor may contribute to the pathogenesis of corneal infection.

摘要

相似文献

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