Human Meningitis-Associated
            <i>Escherichia coli</i>

Kim, Kwang Sik

doi:10.1128/ecosalplus.esp-0015-2015

Cited by 74 publications

(59 citation statements)

References 110 publications

(191 reference statements)

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“…The incidence of bacterial meningitis is about five cases per 100,000 adults per year in developed countries and may be 10 times higher in less developed countries [2]. It estimates that the case fatality rates of the disease range from 5%-25%, and approximately 25%-50% of survivors sustain neurologic sequelae [3]. The blood-brain barrier (BBB) is composed of highly specialized brain microvascular endothelial cells (BMECs), pericytes, and astrocyte endfeet, separates brain tissue from the circulating blood, and maintains homeostasis of the neuronal environment [4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood–Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade

Liu

Huo

et al. 2019

Pathogens

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Bacterial meningitis is currently recognized as one of the most important life-threatening infections of the central nervous system (CNS) with high morbidity and mortality, despite the advancements in antimicrobial treatment. The disruption of blood–brain barrier (BBB) induced by meningitis bacteria is crucial for the development of bacterial meningitis. However, the complete mechanisms involving in the BBB disruption remain to be elucidated. Here, we found meningitic Escherichia coli induction of angiopoietin-like 4 (ANGPTL4) in brain microvascular endothelial cells (BMECs) contributes to BBB disruption via ARHGAP5/RhoA/MYL5 signaling cascade, by the demonstration that ANGPTL4 was significantly upregulated in meningitis E. coli infection of BMECs as well as mice, and treatment of the recombinant ANGPTL4 protein led to an increased permeability of the BBB in vitro and in vivo. Moreover, we found that ANGPTL4 did not affect the expression of tight junction proteins involved in BBB disruption, but it increased the expression of MYL5, which was found to have a negative role on the regulation of barrier function during meningitic E. coli infection, through the activation of RhoA signaling pathway. To our knowledge, this is the first report demonstrating the disruption of BBB induced by ANGPTL4 through the ARHGAP5/RhoA/MYL5 pathway, which largely supports the involvement of ANGPTL4 during meningitic E. coli invasion and further expands the theoretical basis for the mechanism of bacterial meningitis.

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Section: Introductionmentioning

confidence: 99%

Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood–Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade

Liu

Huo

et al. 2019

Pathogens

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“…NMEC is the leading Gram-negative cause of neonatal meningitis cases (Kim, 2016), while UPEC strains are responsible for 75–90% of uncomplicated UTIs and are the leading cause of catheter-associated UTIs (Foxman, 2014; Becknell et al, 2015). In addition, UTIs are a leading cause of E. coli bacteremia (Jackson et al, 2005; Al-Hasan et al, 2010).…”

Section: Diseases In Animals and Humans Caused By Expecsmentioning

confidence: 99%

An Overview of Two-Component Signal Transduction Systems Implicated in Extra-Intestinal Pathogenic E. coli Infections

Breland

Eberly

Hadjifrangiskou

2017

Front. Cell. Infect. Microbiol.

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Extra-intestinal pathogenic E. coli (ExPEC) infections are common in mammals and birds. The predominant ExPEC types are avian pathogenic E. coli (APEC), neonatal meningitis causing E. coli/meningitis associated E. coli (NMEC/MAEC), and uropathogenic E. coli (UPEC). Many reviews have described current knowledge on ExPEC infection strategies and virulence factors, especially for UPEC. However, surprisingly little has been reported on the regulatory modules that have been identified as critical in ExPEC pathogenesis. Two-component systems (TCSs) comprise the predominant method by which bacteria respond to changing environments and play significant roles in modulating bacterial fitness in diverse niches. Recent studies have highlighted the potential of manipulating signal transduction systems as a means to chemically re-wire bacterial pathogens, thereby reducing selective pressure and avoiding the emergence of antibiotic resistance. This review begins by providing a brief introduction to characterized infection strategies and common virulence factors among APEC, NMEC, and UPEC and continues with a comprehensive overview of two-component signal transduction networks that have been shown to influence ExPEC pathogenesis.

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“…Findings on MNEC indicate that the infection starts as a blood infection and then gains access to the central nervous system. A majority of MNEC possess the K1 capsular antigen, and there is a high rate of mortality from the meningitis [12]. This chapter will focus on the six intestinal and the UPEC strains.…”

Section: Pathogenic Strains Of Escherichia Colimentioning

confidence: 99%

Antimicrobial Mechanisms of <i>Escherichia coli</i>

Reygaert¹

2017

≪i>Escherichia Coli

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Increasing antimicrobial resistance in strains of Escherichia coli is having a major impact on the healthcare industry worldwide. The appearance of extended-spectrum β-lactamase (ESBL) and carbapenem-resistant Enterobacteriaceae (CRE) strains has caused clinicians to worry that these strains might become as deadly as methicillin-resistant Staphylococcus aureus (MRSA) strains. It is vital that physicians have resources available to help keep them updated on these bacteria and the potential impact on healthcare. This chapter reviews the major strains of E. coli (intestinal and urinary), along with a review of the virulence factors, main diseases caused, and pertinent pathogenesis. The chapter then discusses antimicrobial therapy, what drugs are effective against these E. coli strains, and the development of resistance to these specific drug classes. Lastly, the molecular aspects of antimicrobial resistance mechanisms in this organism are discussed. This information will be especially helpful for physicians in providing them with a concise review of E. coli and an understanding of what is involved in antimicrobial resistance. Hopefully this information can be used to improve the outcomes for patients with E. coli infections.

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Human Meningitis-Associated Escherichia coli

Cited by 74 publications

References 110 publications

Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood–Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade

Meningitic Escherichia coli Induction of ANGPTL4 in Brain Microvascular Endothelial Cells Contributes to Blood–Brain Barrier Disruption via ARHGAP5/RhoA/MYL5 Signaling Cascade

An Overview of Two-Component Signal Transduction Systems Implicated in Extra-Intestinal Pathogenic E. coli Infections

Antimicrobial Mechanisms of <i>Escherichia coli</i>

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