ArticleCellular microbiology2008
Escherichia coli interaction with human brain microvascular endothelial cells induces signal transducer and activator of transcription 3 association with the C-terminal domain of Ec-gp96, the outer membrane protein A receptor for invasion.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- SARS-CoV-2 nonstructural protein 6 triggers endoplasmic reticulum stress-induced autophagy to degrade STING1.Autophagy · 2023Article
- Biomimetic Lipopolysaccharide-Free Bacterial Outer Membrane-Functionalized Nanoparticles for Brain-Targeted Drug Delivery.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- GP96 Drives Exacerbation of Secondary Bacterial Pneumonia following Influenza A Virus Infection.mBio · 2021Article
- Cell entry of a host-targeting protein of oomycetes requires gp96.Nature communications · 2018Article
- Article
- Host-pathogen interactions in bacterial meningitis.Acta neuropathologica · 2016Review
- Pertussis Toxin Exploits Specific Host Cell Signaling Pathways for Promoting Invasion and Translocation of Escherichia coli K1 RS218 in Human Brain-derived Microvascular Endothelial Cells.The Journal of biological chemistry · 2015Article
- Identification of minimum carbohydrate moiety in N-glycosylation sites of brain endothelial cell glycoprotein 96 for interaction with Escherichia coli K1 outer membrane protein A.Microbes and infection · 2014Article
- Regulation of Toll-like receptor 2 interaction with Ecgp96 controls Escherichia coli K1 invasion of brain endothelial cells.Cellular microbiology · 2013Article
- Listeria monocytogenes triggers the cell surface expression of Gp96 protein and interacts with its N terminus to support cellular infection.The Journal of biological chemistry · 2012Article
- IQGAP1 mediates the disruption of adherens junctions to promote Escherichia coli K1 invasion of brain endothelial cells.Cellular microbiology · 2012Article
- Campylobacter jejuni-mediated induction of CC and CXC chemokines and chemokine receptors in human dendritic cells.Infection and immunity · 2012Article
- IbeA and OmpA of Escherichia coli K1 exploit Rac1 activation for invasion of human brain microvascular endothelial cells.Infection and immunity · 2012Article
- Outer membrane protein A and OprF: versatile roles in Gram-negative bacterial infections.The FEBS journal · 2012Review
- Mechanisms of Candida albicans trafficking to the brain.PLoS pathogens · 2011Article
- Bacterial virulence in the moonlight: multitasking bacterial moonlighting proteins are virulence determinants in infectious disease.Infection and immunity · 2011Review
- Elevated inflammatory response in caveolin-1-deficient mice with Pseudomonas aeruginosa infection is mediated by STAT3 protein and nuclear factor kappaB (NF-kappaB).The Journal of biological chemistry · 2011Article
- Molecular mechanisms of Escherichia coli pathogenicity.Nature reviews. Microbiology · 2010Article
- Nitric oxide/cGMP signalling induces Escherichia coli K1 receptor expression and modulates the permeability in human brain endothelial cell monolayers during invasion.Cellular microbiology · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Our inability to develop new therapeutic strategies to prevent meningitis due to Escherichia coli K1 is attributed to our incomplete understanding of the pathophysiology of the disease. Previously, we demonstrated that outer membrane protein A of E. coli interacts with a gp96 homologue, Ec-gp96, on human brain microvascular endothelial cells (HBMEC) for invasion. However, signalling events mediated by Ec-gp96 that allow internalization of E. coli are incompletely understood. Here, we demonstrate that signal transducer and activator of transcription 3 (Stat3) activation and its interaction with Ec-gp96 were critical for E. coli invasion. The activated Stat3 was colocalized with Ec-gp96 at the actin condensation sites, and overexpressing a dominant negative (DN) form of Stat3 in HBMEC significantly abrogated the invasion. Furthermore, overexpression of Ec-gp96Delta200, the C-terminal 214-amino-acid truncated Ec-gp96, prevented the invasion of E. coli in HBMEC. In contrast, lack of ATP binding by gp96 did not affect the invasion. Overexpression of DN forms of either phosphatidyl inositol-3 kinase (PI3-kinase) subunit p85 or protein kinase C-alpha (PKC-alpha) had no effect on the activation of Stat3 and its association with Ec-gp96, whereas overexpression of DN-Stat3 abolished the activation of both PI3-kinase and PKC-alpha. Together, our findings identified a novel interaction of Stat3 with Ec-gp96, upstream of PI3-kinase and PKC-alpha activation that is required for the invasion of E. coli into HBMEC.
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