Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.

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...

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Autores principales:	Henrik Gradstedt, Federico Iovino, Jetta J E Bijlsma
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9088ad3650a44ad7bcb8eb904b022560
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spelling	oai:doaj.org-article:9088ad3650a44ad7bcb8eb904b0225602021-11-18T07:41:55ZStreptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.1932-620310.1371/journal.pone.0065626https://doaj.org/article/9088ad3650a44ad7bcb8eb904b0225602013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23785439/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Streptococcus 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.Henrik GradstedtFederico IovinoJetta J E BijlsmaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 6, p e65626 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Henrik Gradstedt Federico Iovino Jetta J E Bijlsma Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
description	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.
format	article
author	Henrik Gradstedt Federico Iovino Jetta J E Bijlsma
author_facet	Henrik Gradstedt Federico Iovino Jetta J E Bijlsma
author_sort	Henrik Gradstedt
title	Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
title_short	Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
title_full	Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
title_fullStr	Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
title_full_unstemmed	Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
title_sort	streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/9088ad3650a44ad7bcb8eb904b022560
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Streptococcus pneumoniae invades endothelial host cells via multiple pathways and is killed in a lysosome dependent manner.

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