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dc.contributor.authorMogga, S. J.en_US
dc.contributor.authorMustafa, Tehminaen_US
dc.contributor.authorSviland, Lisbeten_US
dc.contributor.authorNilsen, Runeen_US
dc.date.accessioned2007-01-09T13:59:07Z
dc.date.available2007-01-09T13:59:07Z
dc.date.issued2002-10eng
dc.PublishedScandinavian Journal of Immunology 2002 56(4):383–391
dc.identifier.issn0300-9475
dc.identifier.urihttps://hdl.handle.net/1956/2053
dc.description.abstractMycobacterium tuberculosis (MTB) persists in host macrophages (Mφs) because it has developed mechanisms to escape Mφ killing. In vitro studies have shown that MTB can induce and inhibit apoptosis by causing the expression of Bax and Bcl-2, respectively, suggesting that the infected cells' fate depends on pro- and antiapoptotic signals. In the present study, we investigated the role of Bcl-2 in MTB infection in situ. The aim was to study the pattern and distribution of Bcl-2 and Bax in cellular infiltrates of MTB-infected B6D2F1 hybrid mice and correlate the expression with the presence of MTB antigens (MAgs). Using formalin-fixed lung tissues (n = 45), our results showed a significant difference in the percentage of Mφs stained for Bcl-2 or MAgs and Bax (P < 0.0001). Bcl-2 expression was increased in a population of Mφs and corresponded in intensity, colocalization and percentage with that of MAgs on the same cells, while Bax expression was reduced. In lymphocyte aggregates, Bcl-2 and Bax did not show any differences. We conclude that overexpression of Bcl-2 in Mφs containing MTB may be associated with intracellular survival of the bacilli, thus demonstrating one way by which MTB can escape the host's cellular response and killing.en_US
dc.format.extent3652769 byteseng
dc.format.mimetypeapplication/pdfeng
dc.language.isoengeng
dc.publisherBlackwell Science Ltd.eng
dc.titleIncreased Bcl-2 and Reduced Bax Expression in Infected Macrophages in Slowly Progressive Primary Murine Mycobacterium tuberculosis Infectionen_US
dc.typePeer reviewed
dc.typeJournal article
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2002 Blackwell Science Ltd.
dc.identifier.doihttps://doi.org/10.1046/j.1365-3083.2002.01140.x
dc.subject.nsiVDP::Medisinske Fag: 700::Helsefag: 800nob
dc.subject.nsiVDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk immunologi: 716nob


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