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  4. Τμήμα Ιατρικής
  5. Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ
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Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22315
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dc.contributor.authorAnes, E.en
dc.contributor.authorPeyron, P.en
dc.contributor.authorStaali, L.en
dc.contributor.authorJordao, L.en
dc.contributor.authorGutierrez, M. G.en
dc.contributor.authorKress, H.en
dc.contributor.authorHagedorn, M.en
dc.contributor.authorMaridonneau-Parini, I.en
dc.contributor.authorSkinner, M. A.en
dc.contributor.authorWildeman, A. G.en
dc.contributor.authorKalamidas, S. A.en
dc.contributor.authorKuehnel, M.en
dc.contributor.authorGriffiths, G.en
dc.date.accessioned2015-11-24T19:23:29Z-
dc.date.available2015-11-24T19:23:29Z-
dc.identifier.issn1462-5814-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22315-
dc.rightsDefault Licence-
dc.subjectActins/analysis/metabolismen
dc.subjectAnimalsen
dc.subjectCell Deathen
dc.subjectCell Lineen
dc.subjectCell Survivalen
dc.subjectEndosomes/physiologyen
dc.subjectEnzyme Inhibitors/pharmacologyen
dc.subjectHydrogen-Ion Concentrationen
dc.subjectLysosomes/enzymology/physiologyen
dc.subjectMacrolides/pharmacologyen
dc.subjectMacrophages/cytology/*microbiology/*physiologyen
dc.subjectMiceen
dc.subject*Microbial Viabilityen
dc.subjectModels, Theoreticalen
dc.subjectMycobacterium smegmatis/drug effects/pathogenicity/*physiologyen
dc.subjectNitric Oxide/metabolismen
dc.subjectNitric Oxide Synthase Type II/physiologyen
dc.subjectOrganelles/physiologyen
dc.subjectPhagosomes/chemistry/physiologyen
dc.subjectp38 Mitogen-Activated Protein Kinases/physiologyen
dc.titleDynamic life and death interactions between Mycobacterium smegmatis and J774 macrophagesen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1111/j.1462-5822.2005.00675.x-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/16681836-
heal.identifier.secondaryhttp://onlinelibrary.wiley.com/store/10.1111/j.1462-5822.2005.00675.x/asset/j.1462-5822.2005.00675.x.pdf?v=1&t=h0ko6e68&s=b1680e63a2bca955d89aa676aac63ffa781338e2-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2006-
heal.abstractAfter internalization into macrophages non-pathogenic mycobacteria are killed within phagosomes. Pathogenic mycobacteria can block phagosome maturation and grow inside phagosomes but under some conditions can also be killed by macrophages. Killing mechanisms are poorly understood, although phago-lysosome fusion and nitric oxide (NO) production are implicated. We initiated a systematic analysis addressing how macrophages kill 'non-pathogenic'Mycobacterium smegmatis. This system was dynamic, involving periods of initial killing, then bacterial multiplication, followed by two additional killing stages. NO synthesis represented the earliest killing factor but its synthesis stopped during the first killing period. Phagosome actin assembly and fusion with late endocytic organelles coincided with the first and last killing phase, while recycling of phagosome content and membrane coincided with bacterial growth. Phagosome acidification and acquisition of the vacuolar (V) ATPase followed a different pattern coincident with later killing phases. Moreover, V-ATPase localized to vesicles distinct from classical late endosomes and lysosomes. Map kinase p38 is a crucial regulator of all processes investigated, except NO synthesis, that facilitated the host for some functions while being usurped by live bacteria for others. A mathematical model argues that periodic high and low cellular killing activity is more effective than is a continuous process.en
heal.journalNameCell Microbiolen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
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