ArticlePloS one2014
Impact of calcium signaling during infection of Neisseria meningitidis to human brain microvascular endothelial cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Co-expression of MARCKS and GSDMD pathway genes in tuberculous meningitis: a multi-omics analysis of blood-brain barrier disruption.Frontiers in cellular and infection microbiology · 2026Article
- Transcription Factor Nrf2 Modulates Lipopolysaccharide-Induced Injury in Bovine Endometrial Epithelial Cells.International journal of molecular sciences · 2023Article
- Autophagy MediatesInternational journal of molecular sciences · 2022Article
- Article
- Subversion of Phytomyxae Cell Communication With Surrounding Environment to Control Soilborne Diseases; A Case Study of Cytosolic CaFrontiers in microbiology · 2022Article
- Early growth response 1 (EGR1) activation in initial stages of host-pathogen interactions.Molecular biology reports · 2021Review
- Comparison of different calcium supplementation methods in patients with osteoporosis.Experimental and therapeutic medicine · 2020Article
- Evidence of Calcium Signaling and Modulation of the LmrS Multidrug Resistant Efflux Pump Activity by CaFrontiers in microbiology · 2020Article
- Molecular interactions between Neisseria meningitidis and its human host.Cellular microbiology · 2019Review
- Article
- Neisseria meningitidis Type IV Pili Trigger CaInfection and immunity · 2019Article
- Mitochondria-associated membranes (MAMs) and inflammation.Cell death & disease · 2018Review
- How Shigella Utilizes Ca(2+) Jagged Edge Signals during Invasion of Epithelial Cells.Frontiers in cellular and infection microbiology · 2016Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pili and outer membrane proteins of Neisseria meningitidis (meningococci) facilitate bacterial adhesion and invasion into host cells. In this context expression of meningococcal PilC1 protein has been reported to play a crucial role. Intracellular calcium mobilization has been implicated as an important signaling event during internalization of several bacterial pathogens. Here we employed time lapse calcium-imaging and demonstrated that PilC1 of meningococci triggered a significant increase in cytoplasmic calcium in human brain microvascular endothelial cells, whereas PilC1-deficient meningococci could not initiate this signaling process. The increase in cytosolic calcium in response to PilC1-expressing meningococci was due to efflux of calcium from host intracellular stores as demonstrated by using 2-APB, which inhibits the release of calcium from the endoplasmic reticulum. Moreover, pre-treatment of host cells with U73122 (phospholipase C inhibitor) abolished the cytosolic calcium increase caused by PilC1-expressing meningococci demonstrating that active phospholipase C (PLC) is required to induce calcium transients in host cells. Furthermore, the role of cytosolic calcium on meningococcal adherence and internalization was documented by gentamicin protection assay and double immunofluorescence (DIF) staining. Results indicated that chelation of intracellular calcium by using BAPTA-AM significantly impaired PilC1-mediated meningococcal adherence to and invasion into host endothelial cells. However, buffering of extracellular calcium by BAPTA or EGTA demonstrated no significant effect on meningococcal adherence to and invasion into host cells. Taken together, these results indicate that meningococci induce calcium release from intracellular stores of host endothelial cells via PilC1 and cytoplasmic calcium concentrations play a critical role during PilC1 mediated meningococcal adherence to and subsequent invasion into host endothelial cells.
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