ArticleJournal of neuroinflammation2019
Meningitic Escherichia coli-induced upregulation of PDGF-B and ICAM-1 aggravates blood-brain barrier disruption and neuroinflammatory response.
Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
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- Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
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- Comparative proteomic analysis of Porphyromonas gingivalis challenged human dental pulp stem cells.Scientific reports · 2025Article
- Transition of pseudorabies virus from latency to reactivation state selectively triggered by pathogenic bacteria.Science advances · 2025Article
- Dysregulated miR-1246 and miR-1253 link inflammatory protein markers in plasma to major depressive disorder in female adolescents.Brain, behavior, & immunity - health · 2025Article
- Breaking the fortress: a mechanistic review of meningitis-causing bacteria breaching tactics in blood brain barrier.Cell communication and signaling : CCS · 2025Review
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- Interleukin-22 Contributes to Blood-Brain Barrier Disruption via STAT3/VEGFA Activation inACS infectious diseases · 2024Article
- TGFβ1-induced hedgehog signaling suppresses the immune response of brain microvascular endothelial cells elicited by meningitic Escherichia coli.Cell communication and signaling : CCS · 2024Article
- Benidipine impairs innate immunity converting sublethal to lethal infections in a murine model of spotted fever rickettsiosis.PLoS neglected tropical diseases · 2024Article
- Egr-1 is a key regulator of the blood-brain barrier damage induced by meningitic Escherichia coli.Cell communication and signaling : CCS · 2024Article
- Review
- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Emerging role of non-coding RNAs in neuroinflammation mediated by microglia and astrocytes.Journal of neuroinflammation · 2023Review
- Blood-Brain Barrier Integrity Damage in Bacterial Meningitis: The Underlying Link, Mechanisms, and Therapeutic Targets.International journal of molecular sciences · 2023Review
- Hcp Proteins of the Type VI Secretion System Promote Avian PathogenicLife (Basel, Switzerland) · 2022Article
- Transcriptional landscape of human neuroblastoma cells in response to SARS-CoV-2.BMC neuroscience · 2022Article
- SARS-CoV-2 productively infects human brain microvascular endothelial cells.Journal of neuroinflammation · 2022Article
- MeningiticFrontiers in cellular neuroscience · 2022Article
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12 authors.
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Abstract
backgroundBlood-brain barrier (BBB) disruption and neuroinflammation are considered key mechanisms of pathogenic Escherichia coli invasion of the brain. However, the specific molecules involved in meningitic E. coli-induced BBB breakdown and neuroinflammatory response remain unclear. Our previous RNA-sequencing data from human brain microvascular endothelial cells (hBMECs) revealed two important host factors: platelet-derived growth factor-B (PDGF-B) and intercellular adhesion molecule-1 (ICAM-1), which were significantly upregulated in hBMECs after meningitic E. coli infection. Whether and how PDGF-B and ICAM-1 contribute to the development of E. coli meningitis are still unclear.
methodsThe western blot, real-time PCR, enzyme-linked immunosorbent assay, immunohistochemistry, and immunofluorescence were applied to verify the significant induction of PDGF-B and ICAM-1 by meningitic E. coli in vivo and in vitro. Evan's blue assay and electric cell-substrate impedance sensing assay were combined to identify the effects of PDGF-B on BBB permeability. The CRISPR/Cas9 technology, cell-cell adhesion assay, and electrochemiluminescence assay were used to investigate the role of ICAM-1 in neuroinflammation subversion.
resultsWe verified the significant induction of PDGF-B and ICAM-1 by meningitic E. coli in mouse as well as monolayer hBMECs models. Functionally, we showed that the increase of PDGF-B may directly enhance the BBB permeability by decreasing the expression of tight junction proteins, and the upregulation of ICAM-1 contributed to neutrophils or monocytes recruitment as well as neuroinflammation subversion in response to meningitic E. coli infection.
conclusionsOur findings demonstrated the roles of PDGF-B and ICAM-1 in mediating bacterial-induced BBB damage as well as neuroinflammation, providing new concepts and potential targets for future prevention and treatment of bacterial meningitis.
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