ArticlePloS one2013
Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Lysosome and Cytoskeleton Pathways Are Robustly Enriched in the Blood of Septic Patients: A Meta-Analysis of Transcriptomic Data.Mediators of inflammation · 2015Pooled it
- Pneumococcal vaccines: understanding centers for disease control and prevention recommendations.Annals of the American Thoracic Society · 2014Trial
- Exploring the role of infectious pathogens in Alzheimer's disease neuroinflammation.Frontiers in cellular and infection microbiology · 2026Review
- Alveolar-capillary endocytosis and trafficking in acute lung injury and acute respiratory distress syndrome.Frontiers in immunology · 2024Review
- The oxidative stress response ofFrontiers in microbiology · 2023Review
- Differential Ubiquitination as an Effective Strategy Employed by the Blood-Brain Barrier for Prevention of Bacterial Transcytosis.Journal of bacteriology · 2022Article
- Article
- Review
- Endothelial Cell Protein C Receptor Deficiency AttenuatesAmerican journal of respiratory cell and molecular biology · 2021Article
- Arginine Decarboxylase Is Essential for Pneumococcal Stress Responses.Pathogens (Basel, Switzerland) · 2021Article
- Review
- Article
- New insights into pediatric community-acquired pneumonia gained from untargeted metabolomics: A preliminary study.Pediatric pulmonology · 2020Article
- Pneumococcal Encounter With the Blood-Brain Barrier Endothelium.Frontiers in cellular and infection microbiology · 2020Review
- Nicotine Reduces Human Brain Microvascular Endothelial Cell Response toFrontiers in cellular and infection microbiology · 2020Article
- Heterogeneity in pneumolysin expression governs the fate of Streptococcus pneumoniae during blood-brain barrier trafficking.PLoS pathogens · 2018Article
- Article
- Budesonide and fluticasone propionate differentially affect the airway epithelial barrier.Respiratory research · 2016Article
- Streptococcus pneumoniae induces autophagy through the inhibition of the PI3K-I/Akt/mTOR pathway and ROS hypergeneration in A549 cells.PloS one · 2015Article
- Platelet endothelial cell adhesion molecule-1, a putative receptor for the adhesion of Streptococcus pneumoniae to the vascular endothelium of the blood-brain barrier.Infection and immunity · 2014Article
Corrections and comments
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Streptococcus pneumoniae is one of the major causative agents of pneumonia, sepsis, meningitis and other morbidities. In spite of its heavy disease burden, surprisingly little is known about the mechanisms involved in the switch of life style, from commensal colonizer of the nasopharynx to invasive pathogen. In vitro experiments, and mouse models have shown that S. pneumoniae can be internalized by host cells, which coupled with intracellular vesicle transport through the cells, i.e. transcytosis, is suggested to be the first step of invasive disease. To further dissect the process of S. pneumoniae internalization, we chemically inhibited discrete parts of the cellular uptake system. We show that this invasion of the host cells was facilitated via both clathrin- and caveolae-mediated endocytosis. After internalization we demonstrated that the bulk of the internalized S. pneumoniae was killed in the lysosome. Interestingly, inhibition of the lysosome altered transcytosis dynamics as it resulted in an increase in the transport of the internalized bacteria out of the cells via the basal side. These results show that uptake of S. pneumoniae into host cells occurs via multiple pathways, as opposed to the often proposed view of invasion being dependent on specific, and singular receptor-mediated endocytosis. This indicates that the endothelium not only has a critical role as a physical barrier against S. pneumoniae in the blood stream, but also in degrading S. pneumonia cells that have adhered to, and invaded the endothelial cells.
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