Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/44361
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dc.contributor.authorCohen, A-
dc.contributor.authorTroib, S-
dc.contributor.authorDotan, S-
dc.contributor.authorNajmuldeen, H-
dc.contributor.authorYesilkaya, H-
dc.contributor.authorKushnir, T-
dc.contributor.authorShagan, M-
dc.contributor.authorPortnoi, M-
dc.contributor.authorNachmani, H-
dc.contributor.authorBenisty, R-
dc.contributor.authorTal, M-
dc.contributor.authorEllis, R-
dc.contributor.authorChalifa-Caspi, V-
dc.contributor.authorDagan, R-
dc.contributor.authorNebenzahl, YM-
dc.date.accessioned2019-06-11T15:06:55Z-
dc.date.available2019-06-11T15:06:55Z-
dc.date.issued2019-03-12-
dc.identifier.citationScientific Reports, 2019, 9, Article number: 4295en
dc.identifier.urihttps://www.nature.com/articles/s41598-019-40779-0en
dc.identifier.urihttp://hdl.handle.net/2381/44361-
dc.descriptionSupplementary information accompanies this paper at https://doi.org/10.1038/s41598-019-40779-0.en
dc.description.abstractTrigger factor (TF) has a known cytoplasmic function as a chaperone. In a previous study we showed that pneumococcal TF is also cell-wall localized and this finding combined with the immunogenic characteristic of TF, has led us to determine the vaccine potential of TF and decipher its involvement in pneumococcal pathogenesis. Bioinformatic analysis revealed that TF is conserved among pneumococci and has no human homologue. Immunization of mice with recombinant (r)TF elicited a protective immune response against a pneumococcal challenge, suggesting that TF contributes to pneumococcal pathogenesis. Indeed, rTF and an anti-rTF antiserum inhibited bacterial adhesion to human lung derived epithelial cells, indicating that TF contributes to the bacterial adhesion to the host. Moreover, bacteria lacking TF demonstrated reduced adhesion, in vitro, to lung-derived epithelial cells, neural cells and glial cells. The reduced adhesion could be restored by chromosomal complementation. Furthermore, bacteria lacking TF demonstrated significantly reduced virulence in a mouse model. Taken together, the ability of rTF to elicit a protective immune response, involvement of TF in bacterial adhesion, conservation of the protein among pneumococcal strains and the lack of human homologue, all suggest that rTF can be considered as a future candidate vaccine with a much broader coverage as compared to the currently available pneumococcal vaccines.en
dc.description.sponsorshipThis work was supported by grants from the Israeli Ministry of Health numbers 4776 and 5540, 3000003867, from the Center of Emerging Diseases #2506, from the Israel Academy of Science 613/04, The Israel Ministry of Commerce and Industry to NasVax Ltd., European Community 7th FP: CAREPNEUMO 223111, from BGNegev Biotechnology to YMN.en
dc.language.isoenen
dc.publisherNature Research (part of Springer Nature)en
dc.relation.urihttps://www.ncbi.nlm.nih.gov/pubmed/30862841-
dc.rightsCopyright © the authors, 2019. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en
dc.titleStreptococcus pneumoniae Cell Wall-Localized Trigger Factor Elicits a Protective Immune Response and Contributes to Bacterial Adhesion to the Host.en
dc.typeJournal Articleen
dc.identifier.doi10.1038/s41598-019-40779-0-
dc.identifier.eissn2045-2322-
dc.identifier.pii10.1038/s41598-019-40779-0-
dc.description.statusPeer-revieweden
dc.description.versionPublisher Versionen
dc.type.subtypeJournal Article-
pubs.organisational-group/Organisationen
pubs.organisational-group/Organisation/COLLEGE OF LIFE SCIENCESen
pubs.organisational-group/Organisation/COLLEGE OF LIFE SCIENCES/School of Medicineen
pubs.organisational-group/Organisation/COLLEGE OF LIFE SCIENCES/School of Medicine/Department of Infection, Immunity and Inflammationen
dc.dateaccepted2018-10-24-
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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