Abstract:
:The vast majority of cases of gram-negative meningitis in neonates are caused by K1-encapsulated Escherichia coli. The role of the K1 capsule in the pathogenesis of E. coli meningitis was examined with an in vivo model of experimental hematogenous E. coli K1 meningitis and an in vitro model of the blood-brain barrier. Bacteremia was induced in neonatal rats with the E. coli K1 strain C5 (O18:K1) or its K1(-) derivative, C5ME. Subsequently, blood and cerebrospinal fluid (CSF) were obtained for culture. Viable bacteria were recovered from the CSF of animals infected with E. coli K1 strains only; none of the animals infected with K1(-) strains had positive CSF cultures. However, despite the fact that their cultures were sterile, the presence of O18 E. coli was demonstrated immunocytochemically in the brains of animals infected with K1(-) strains and was seen by staining of CSF samples. In vitro, brain microvascular endothelial cells (BMEC) were incubated with K1(+) and K1(-) E. coli strains. The recovery of viable intracellular organisms of the K1(+) strain was significantly higher than that for the K1(-) strain (P = 0.0005). The recovery of viable intracellular K1(-) E. coli bacteria was increased by cycloheximide treatment of BMEC (P = 0.0059) but was not affected by nitric oxide synthase inhibitors or oxygen radical scavengers. We conclude that the K1 capsule is not necessary for the invasion of bacteria into brain endothelial cells but is responsible for helping to maintain bacterial viability during invasion of the blood-brain barrier.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Hoffman JA,Wass C,Stins MF,Kim KSdoi
10.1128/IAI.67.7.3566-3570.1999keywords:
subject
Has Abstractpub_date
1999-07-01 00:00:00pages
3566-70issue
7eissn
0019-9567issn
1098-5522journal_volume
67pub_type
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journal_title:Infection and immunity
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doi:10.1128/IAI.50.1.136-141.1985
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journal_title:Infection and immunity
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doi:10.1128/IAI.59.5.1592-1598.1991
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abstract::The intraerythrocytic apicomplexan Babesia microti, the primary causative agent of human babesiosis, is a major public health concern in the United States and elsewhere. Apicomplexans utilize a multiprotein complex that includes a type I membrane protein called apical membrane antigen 1 (AMA1) to invade host cells. We...
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journal_title:Infection and immunity
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doi:10.1128/IAI.26.1.254-261.1979
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.10.5.1003-1009.1974
更新日期:1974-11-01 00:00:00
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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doi:10.1128/IAI.65.7.2629-2639.1997
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.43.1.402-406.1984
更新日期:1984-01-01 00:00:00
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journal_title:Infection and immunity
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doi:10.1128/IAI.66.8.3918-3924.1998
更新日期:1998-08-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.59.3.949-954.1991
更新日期:1991-03-01 00:00:00
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journal_title:Infection and immunity
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abstract::Borrelia burgdorferi sensu stricto is the major causative agent of Lyme disease in the United States, while B. garinii and B. afzelii are more prevalent in Europe. The highly complex genome of B. burgdorferi is comprised of a linear chromosome and a large number of variably sized linear and circular plasmids. Many pla...
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.27.2.525-531.1980
更新日期:1980-02-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.55.1.16-23.1987
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journal_title:Infection and immunity
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abstract::Three strains of anaerobic, dextranase-producing, gram-positive, rod-shaped bacteria were isolated from human dental plaque associated with root carious lesions. The isolates produced a molar ratio of acetate to lactate from glucose fermentation ranging from 1.1 to 1.9. Each strain also produced fructose-6-phosphate p...
journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.42.2.716-720.1983
更新日期:1983-11-01 00:00:00
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journal_title:Infection and immunity
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doi:10.1128/IAI.73.11.7657-7668.2005
更新日期:2005-11-01 00:00:00
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更新日期:2007-06-01 00:00:00