Interactions of Neuropathogenic Escherichia coli K1 (RS218) and Its Derivatives Lacking Genomic Islands with Phagocytic Acanthamoeba castellanii and Nonphagocytic Brain Endothelial Cells
Table 1
Summary of E. coli K1 RS218 derived islands (RDI’s) and its genomic islands mutants tested in the present study.
E. coli K1
Identity
Function and potential virulence factor
K1 (RS218)
Isolate from a meningitis patient.
Plasmid cured RS218
Plasmid-free strain
RS218 complemented with HB101 DNA
Strain, in which genomic deletion (black hole) observed in RS218 was filled with respective DNA from HB101
RDI 1
Invasins (IcmF and IcmH).
RDI 2
Prophage genes.
RDI 4
Adhesins (S fimbriae, antigen 43). Protein secretion system (T5SS for antigen 43). Iron uptake system (Iro system and hmu system).
RDI 9
Iron uptake system (Ybt system).
RDI 10
Toxins (peptide toxin).
RDI 12
Other virulence factors (sia operon). Prophage genes.
RDI 14
Prophage genes.
RDI 15
Metabolism (sugar metabolism).
RDI 16
Protein secretion system (T2SS). Other virulence factors (K1 capsule biosynthesis).
RDI 17
Metabolism (phosphor-sugar metabolism).
RDI 18
Prophage genes.
RDI 21
Adhesins (P fimbriae, F17-like fimbriae, non-fimbrial adhesins, Hek and hemagglutinin). Protein secretion system (T1SS for hemolysin). Invasins (CNF1). Metabolism (D-serine catabolism).
RDI 22
Invasins (IbeA). Toxins (α-hemolysin). Metabolism (dihydroxyacetone, glycerol, and glyoxylate metabolism).