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Beneficial effect of chronic Staphylococcus aureus infection in a model of multiple sclerosis is mediated through the secretion of extracellular adherence protein

dc.contributor.authorKumar, Prateek
dc.contributor.authorKretzschmar, Benedikt
dc.contributor.authorHerold, Sabine
dc.contributor.authorNau, Roland
dc.contributor.authorKreutzfeldt, Mario
dc.contributor.authorSchütze, Sandra
dc.contributor.authorBähr, Mathias
dc.contributor.authorHein, Katharina
dc.date.accessioned2015-02-11T04:27:39Z
dc.date.accessioned2015-05-21T13:02:04Z
dc.date.available2015-02-11T04:27:39Z
dc.date.available2015-05-21T13:02:04Z
dc.date.issued2015
dc.identifier.urihttp://resolver.sub.uni-goettingen.de/purl?gs-1/11595
dc.description.abstractBackground Bacterial infections have been assumed to worsen multiple sclerosis (MS) disease symptoms and to lead to increased neurodegeneration. However, the underlying biological mechanisms for these effects are complex and poorly understood. Here, we assessed the disease-modulating effects of chronic infection with Staphylococcus aureus, a common human pathogen, on the clinical course and the extent of neurodegeneration in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Methods To conduct this study, we established a persistent chronic infection in female brown Norway rats by inoculating Staphylococcus aureus (S. aureus) bacteria in a subcutaneously implanted tissue cages. Results In this study, we observed that the introduction of a localized S. aureus infection during the subclinical phase of EAE induced a chronic systemic inflammatory response, consisting of increased T- and B-cell counts and systemic production of proinflammatory cytokines. Unexpectedly, the S. aureus infection completely prevented the development of clinical EAE, and markedly reduced inflammatory infiltration and demyelination of the optic nerve, while it increased the number of surviving retinal neurons. Using a S. aureus strain that lacked the extracellular adherence protein (Eap), we determined that the extracellular adherence protein is at least partially responsible for the inhibitory effect of S. aureus infection on autoimmune inflammation of the central nervous system. Conclusions Our results demonstrate for the first time that chronic infection with S. aureus has a beneficial effect on EAE, indicating a dual role of infection in the pathogenesis of MS. We also showed that secretion of Eap by S. aureus plays a major role in preventing autoimmune inflammation of the CNS. Moreover, we identified Eap as a factor responsible for this protective effect.
dc.language.isoeng
dc.identifier.bibliographicCitationJournal of Neuroinflammation. 2015 Feb 03;12(1):22
dc.rightsopenAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0
dc.titleBeneficial effect of chronic Staphylococcus aureus infection in a model of multiple sclerosis is mediated through the secretion of extracellular adherence protein
dc.typejournalArticle
dc.identifier.doi10.1186/s12974-015-0241-8
dc.type.versionpublishedVersion
dc.date.updated2015-02-11T04:27:40Z
dc.rights.holderPrateek Kumar et al.; licensee BioMed Central Ltd.
dc.bibliographicCitation.volume12
dc.bibliographicCitation.issue1
dc.type.subtypejournalArticle
dc.identifier.pmid25644616
dc.bibliographicCitation.articlenumber22
dc.description.statuspeerReviewed
dc.bibliographicCitation.journalJournal of Neuroinflammation


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