Pseudomonas aeruginosa strains with lipopolysaccharide defects exhibit reduced intracellular viability after invasion of corneal epithelial cells.
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.
Evans
David
D
Morton D. Sarver Laboratory for Cornea and Contact Lens Research, School of Optometry, University of California at Berkeley, Berkeley, CA 94720, USA.
Kuo
Tracy
T
Kwong
Mary
M
Van
Rajana
R
Fleiszig
Suzanne
S
D000818:Animals; D018929:Cell Culture Techniques; D019573:Epithelium, Corneal / Q000382:microbiology*; D008070:Lipopolysaccharides / Q000378:metabolism*; D009154:Mutation; D011550:Pseudomonas aeruginosa / Q000235:genetics / Q000472:pathogenicity*; D011817:Rabbits; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics / Q000502:physiology*
D008070:Lipopolysaccharides; D037521:Virulence Factors