Interactions of Neuropathogenic Escherichia coli Kl (RS218) and Its Derivatives Lacking Genomic Islands with Phagocytic Acanthamoeha castellanii and Nonphagocytic Brain Endothelial Cells

摘要

Here we determined the role of various genomic islands in E. coli Kl interactions with phagocytic A. castellanii and nonphagocytic brain microvascular endothelial cells. The findings revealed that the genomic islands deletion mutants of RS218 related to toxins (peptide toxin, a-hemolysin), adhesins (P fimbriae, F17-like fimbriae, nonfimbrial adhesins, Hek, and hemagglutinin), protein secretion system (T1SS for hemolysin), invasins (IbeA, CNF1), metabolism (D-serine catabolism, dihydroxyacetone, glycerol, and glyoxiate metabolism) showed reduced interactions with both A. castellanii and brain microvascular endothelial cells. Interestingly, the deletion of RS218-derived genomic island 21 containing adhesins (P fimbriae, F17-like fimbriae, nonfimbrial adhesins, Hek, and hemagglutinin), protein secretion system (TlSS for hemolysin), invasins (CNF1), metabolism (D-serine catabolism) abolished E. coli Kl-mediated HBMEC cytotoxicity in a CNFl-independent manner. Therefore, the characterization of these genomic islands should reveal mechanisms of evolutionary gain for E. coli Kl pathogenicity.