{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Letsiou E"],"funding":["ERS-EU RESPIRE2 Marie Skłodowska-Curie Research Fellowship","German Research Foundation","German Ministry of Education and Research"],"pagination":["9529"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8100145"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11(1)"],"pubmed_abstract":["Microvesicles (MVs) are cell-derived extracellular vesicles that have emerged as markers and mediators of acute lung injury (ALI). One of the most common pathogens in pneumonia-induced ALI is Streptococcus pneumoniae (Spn), but the role of MVs during Spn lung infection is largely unknown. In the first line of defense against Spn and its major virulence factor, pneumolysin (PLY), are the alveolar epithelial cells (AEC). In this study, we aim to characterize MVs shed from PLY-stimulated AEC and explore their contribution in mediating crosstalk with neutrophils. Using in vitro cell and ex vivo (human lung tissue) models, we demonstrated that Spn in a PLY-dependent manner stimulates AEC to release increased numbers of MVs. Spn infected mice also had higher levels of epithelial-derived MVs in t"],"journal":["Scientific reports"],"pubmed_title":["Microvesicles released from pneumolysin-stimulated lung epithelial cells carry mitochondrial cargo and suppress neutrophil oxidative burst."],"pmcid":["PMC8100145"],"funding_grant_id":["CAPSyS (01ZX1304B), SYMPATH (FKZ 01ZX1906A) and PROVID project (FKZ 01KI20160A)","MCF 9019-2015","SFB-TR84 C6 and C9"],"pubmed_authors":["Muller-Redetzky HC","Fatykhova D","Hocke AC","Felten M","Mitchell TJ","Witzenrath M","Teixeira Alves LG","Letsiou E"],"additional_accession":[]},"is_claimable":false,"name":"Microvesicles released from pneumolysin-stimulated lung epithelial cells carry mitochondrial cargo and suppress neutrophil oxidative burst.","description":"Microvesicles (MVs) are cell-derived extracellular vesicles that have emerged as markers and mediators of acute lung injury (ALI). One of the most common pathogens in pneumonia-induced ALI is Streptococcus pneumoniae (Spn), but the role of MVs during Spn lung infection is largely unknown. In the first line of defense against Spn and its major virulence factor, pneumolysin (PLY), are the alveolar epithelial cells (AEC). In this study, we aim to characterize MVs shed from PLY-stimulated AEC and explore their contribution in mediating crosstalk with neutrophils. Using in vitro cell and ex vivo (human lung tissue) models, we demonstrated that Spn in a PLY-dependent manner stimulates AEC to release increased numbers of MVs. Spn infected mice also had higher levels of epithelial-derived MVs in t","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2025-04-21T18:23:56.076Z","creation":"2025-04-05T17:12:50.709Z"},"accession":"S-EPMC8100145","cross_references":{"pubmed":["33953279"],"doi":["10.1038/s41598-021-88897-y"]}}