Please use this identifier to cite or link to this item: https://doi.org/10.4049/jimmunol.0902663
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dc.titleSuppression of host innate immune response by Burkholderia pseudomallei through the virulence factor TssM
dc.contributor.authorTan, K.S.
dc.contributor.authorChen, Y.
dc.contributor.authorLim, Y.-C.
dc.contributor.authorTan, G.-Y.G.
dc.contributor.authorLiu, Y.
dc.contributor.authorLim, Y.-T.
dc.contributor.authorMacAry, P.
dc.contributor.authorGan, Y.-H.
dc.date.accessioned2014-11-26T07:48:40Z
dc.date.available2014-11-26T07:48:40Z
dc.date.issued2010-05-01
dc.identifier.citationTan, K.S., Chen, Y., Lim, Y.-C., Tan, G.-Y.G., Liu, Y., Lim, Y.-T., MacAry, P., Gan, Y.-H. (2010-05-01). Suppression of host innate immune response by Burkholderia pseudomallei through the virulence factor TssM. Journal of Immunology 184 (9) : 5160-5171. ScholarBank@NUS Repository. https://doi.org/10.4049/jimmunol.0902663
dc.identifier.issn00221767
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/109675
dc.description.abstractBurkholderia pseudomallei is a Gram-negative saprophyte that is the causative agent of melioidosis, a severe infectious disease endemic in Northern Australia and Southeast Asia. This organism has sparked much scientific interest in the West because of its classification as a potential bioterrorism agent by the U.S. Centers for Disease Control and Prevention. However, relatively little is known about its pathogenesis. We demonstrate that B. pseudomallei actively inhibits NF-κB and type I IFN pathway activation, thereby downregulating host inflammatory responses. We found the virulence factor TssM to be responsible for this activity. TssM interferes with the ubiquitination of critical signaling intermediates, including TNFR-associated factor-3, TNFR-associated factor-6, and IκBα. The expression but not secretion of TssM is regulated by the type III secretion system. We demonstrate that TssM is important for B. pseudomallei infection in vivo as inflammation in the tssM mutant-infected mice is more severe and corresponds to a more rapid death compared with wild-type bacteria-infected mice. Abs to TssM can be detected in the sera of melioidosis patients, indicating that TssM is functionally expressed in vivo and thus could contribute to bacterial pathogenesis in human melioidosis. Copyright © 2010 by The American Association of Immunologists, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.4049/jimmunol.0902663
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentBIOCHEMISTRY
dc.description.doi10.4049/jimmunol.0902663
dc.description.sourcetitleJournal of Immunology
dc.description.volume184
dc.description.issue9
dc.description.page5160-5171
dc.description.codenJOIMA
dc.identifier.isiut000277093000069
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