scholarly journals Escherichia coli Binding to and Invasion of Brain Microvascular Endothelial Cells Derived from Humans and Rats of Different Ages

1999 ◽  
Vol 67 (10) ◽  
pp. 5522-5525 ◽  
Author(s):  
Monique F. Stins ◽  
Prasadarao V. Nemani ◽  
Carol Wass ◽  
Kwang Sik Kim
Keyword(s):  
Escherichia Coli ◽  
Neonatal Period ◽  
Microvascular Endothelial Cell ◽  
Age Dependency ◽  
Brain Microvascular Endothelial Cell ◽  
E Coli ◽  
Different Ages ◽  
Old Adult ◽  
Old Rats ◽  
Microvascular Endothelial

ABSTRACT Escherichia coli meningitis commonly occurs in the neonatal period, but the basis of this age dependency is unclear. We have previously identified two types of E. coli-brain microvascular endothelial cell (BMEC) interactions contributing toE. coli traversal of the blood-brain barrier (i.e., binding and invasion). The present study examined whether the age dependency ofE. coli meningitis stemmed from differences in the capacities of neonatal and adult BMECs to interact with E. coli. BMECs were isolated from rats of different ages (10 days, 20 days and 3 months) as well as from humans of different ages (fetuses, 4- to 7-year-old children, and a 35-year-old adult, and 60- to 85-year-old geriatrics). The bindings of E. coli to young and old rat BMECs were similar. Also, the abilities of E. coli to invade BMECs were similar for BMECs derived from young and old rats and from human fetuses, children, adults, and geriatrics. These findings suggest that the predominance of E. colimeningitis in neonates is not likely due to greater binding and invasion capacities of newborn compared to adult BMECs.

Vacuolisation of human microvascular endothelial cells by enterohaemorrhagic Escherichia coli

2009 ◽  
Vol 102 (12) ◽  
pp. 1080-1092 ◽  
Author(s):  
Lilo Greune ◽  
Björn Kemper ◽  
Ulrich Dobrindt ◽  
Joyce Geelen ◽  
Kwang Kim ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Endothelial Cells ◽  
Neutral Red ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelial Cell ◽  
Microvascular Endothelium ◽  
Vacuolating Cytotoxin ◽  
E Coli ◽  
Enterohaemorrhagic Escherichia Coli ◽  
Microvascular Endothelial

SummaryEnterohaemorrhagic Escherichia coli (EHEC) cause haemolytic uraemic syndrome (HUS),a thrombotic microangiopathy resulting from endothelial injury in the renal glomeruli and other organs. EHEC virulence factors that damage the microvascular endothelium play therefore major roles in the pathogenesis of HUS.We identified an EHEC strain that vacuolates and kills primary human glomerular microvascular endothelial cells (GMVECs) and a human brain microvascular endothelial cell (HBMEC) line. Because the vacuolating effect closely resembles those elicited on other cells by the vacuolating cytotoxin of Helicobacter pylori (VacA), we designated the factor responsible for this effect EHEC vacuolating cytotoxin (EHEC-Vac). EHEC-Vac (a secreted non-serine protease protein) binds to HBMECs rapidly and irreversibly, vacuolates within 30 min after exposure and the effect is maximally apparent at 48 h. Despite the vacuolisation, HBMECs survive for several days before they undergo necrosis. Electron and immunofluorescence microscopy demonstrate that the vacuoles induced by EHEC-Vac originate from lysosomes.Accordingly, they stain with neutral red indicating an acidic microenvironment. Similar to VacA, the EHEC-Vac-mediated vacuolisation is both prevented and reverted by the vacuolar proton pump inhibitor bafilomycin A1, suggesting a similar mechanism of vacuole formation by these toxins. Despite the similarity of phenotypes elicited by EHEC-Vac and VacA, genomic DNA from the EHEC-Vac-producing strain failed to hybridise to a vacA probe, as well as to probes derived from presently known E. coli vacuolating toxins.Through its microvascular endothelium-injuring potential combined with the ability to induce interleukin 6 release from these cells EHEC-Vac might contribute to the pathogenesis of HUS.

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