Interactions of NeuropathogenicEscherichia coliK1 (RS218) and Its Derivatives Lacking Genomic Islands with PhagocyticAcanthamoeba castellaniiand Nonphagocytic Brain Endothelial Cells

Abstract

Here we determined the role of various genomic islands in E. coli K1 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, α-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 glyoxylate 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 (T1SS for hemolysin), invasins (CNF1), metabolism (D-serine catabolism) abolished E. coli K1-mediated HBMEC cytotoxicity in a CNF1-independent manner. Therefore, the characterization of these genomic islands should reveal mechanisms of evolutionary gain for E. coli K1 pathogenicity.

Divalent metal cations potentiate the predatory capacity of amoeba forCryptococcus neoformans

“…For example, A castellanii interactions with Vibrio cholerae (40), Aspergillus fumigatus (10), Pseudomonas aeruginosa (41), Corynebacterium spp . (41) and E. coli (42), were studied in peptone yeast extract and glucose (PYG) media while interactions with Campylobacter jejuni (43), were done in ‘amoeba buffer’ that included Ca 2+ and Mg 2+ cations and Bacillus anthracis (44) in autoclaved creek water supplemented with divalent cations. Given the powerful effects of divalent cations on amoeba function comparisons across studies need to take into account the possibility that differences in Ca 2+ and Mg 2+ could affect experimental outcomes.…”

Lactobacillus rhamnosus GG supernatant enhance neonatal resistance to systemic Escherichia coli K1 infection by accelerating development of intestinal defense

“…Understanding and delineating the mechanism and the course of neonatal E. coli K1 sepsis and meningitis could provide a foundation for developing novel prophylactics. Although the exact mechanisms of E. coli K1–induced pathogenicity remain unclear, the natural course of E. coli K1 infection involving a series of steps as following have been established in detail: (a) gastrointestinal colonization by E. coli K1, often vertical transmission from the mother’s birth canal during delivery 7 8 ; (b) E. coli K1 crosses the intestinal mucosal barrier and escape into the blood stream, then survive and multiply in the blood resulting in bacteraemia 9 ; (c) finally, the bacteria transmigrate across the blood-brain barrier (BBB) and invade the central nervous system resulting in inflammatory responses and pathophysiological alterations such as pleocytosis and BBB injury that ultimately leads to neurological complications or death 10 . These steps indicate that the blockage of bacterial adherence to enterocyte and translocation across the intestinal barrier into the bloodstream would be a potential approach to prevent neonatal E. coli K1 sepsis and meningitis.…”

Targeting cyst wall is an effective strategy in improving the efficacy of marketed contact lens disinfecting solutions against Acanthamoeba castellanii cysts

“…Acanthamoeba keratitis is characterized by 16 blurred vision, sensitivity to light, conjunctivitis, eye lid swelling, 17 and reddened eye with watery discharge, and severe pain [7]. 18 Approximately 85-88% cases of Acanthamoeba keratitis are 19 associated with the use of contact lens and hence contact lens 20 wearers are at increased risk of this infection [8,9]. Acanthamoeba 21 keratitis is often linked to contact lens disinfectants that fail to 22 effectively decontaminate contact lens.…”