Role for the Burkholderia pseudomallei Type Three Secretion System Cluster 1 bpscN gne in vrulence

Tanya D'Cruze, Lan Gong, Puthayalai Treerat, Georg Ramm, John Boyce, Mark Prescott, Ben Adler, Rodney Devenish

Research output: Contribution to journalArticleResearchpeer-review

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Abstract

Burkholderia pseudomallei, the causal agent of melioidosis, employs a number of virulence factors during its infection of mammalian cells. One such factor is the Type Three Secretion System (TTSS), which is proposed to mediate the transport and secretion of bacterial effector molecules directly into host cells. The B. pseudomallei genome contains three TTSS gene clusters (designated TTSS1, TTSS2 and TTSS3). Previous research has indicated that neither TTSS1 nor TTSS2 are involved in B. pseudomallei virulence in a hamster infection model. We have characterised a B. pseudomallei mutant lacking expression of the predicted TTSS1 ATPase encoded by bpscN. This mutant was significantly attenuated for virulence in a respiratory melioidosis mouse model of infection. In addition, analyses in vitro showed diminished survival and replication in RAW264.7 cells, an increased level of co-localisation with the autophagy marker protein LC3, but an unhindered ability to escape from phagosomes. Taken together, these data provide evidence that the TTSS1 bpscN gene product plays an important role in the intracellular survival of B. pseudomallei and the pathogenesis of murine infection.
Original languageEnglish
Pages (from-to)3659 - 3664
Number of pages6
JournalInfection and Immunity
Volume79
Issue number9
DOIs
Publication statusPublished - 2011

Cite this

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title = "Role for the Burkholderia pseudomallei Type Three Secretion System Cluster 1 bpscN gne in vrulence",
abstract = "Burkholderia pseudomallei, the causal agent of melioidosis, employs a number of virulence factors during its infection of mammalian cells. One such factor is the Type Three Secretion System (TTSS), which is proposed to mediate the transport and secretion of bacterial effector molecules directly into host cells. The B. pseudomallei genome contains three TTSS gene clusters (designated TTSS1, TTSS2 and TTSS3). Previous research has indicated that neither TTSS1 nor TTSS2 are involved in B. pseudomallei virulence in a hamster infection model. We have characterised a B. pseudomallei mutant lacking expression of the predicted TTSS1 ATPase encoded by bpscN. This mutant was significantly attenuated for virulence in a respiratory melioidosis mouse model of infection. In addition, analyses in vitro showed diminished survival and replication in RAW264.7 cells, an increased level of co-localisation with the autophagy marker protein LC3, but an unhindered ability to escape from phagosomes. Taken together, these data provide evidence that the TTSS1 bpscN gene product plays an important role in the intracellular survival of B. pseudomallei and the pathogenesis of murine infection.",
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Role for the Burkholderia pseudomallei Type Three Secretion System Cluster 1 bpscN gne in vrulence. / D'Cruze, Tanya; Gong, Lan; Treerat, Puthayalai; Ramm, Georg; Boyce, John; Prescott, Mark; Adler, Ben; Devenish, Rodney.

In: Infection and Immunity, Vol. 79, No. 9, 2011, p. 3659 - 3664.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

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AU - D'Cruze, Tanya

AU - Gong, Lan

AU - Treerat, Puthayalai

AU - Ramm, Georg

AU - Boyce, John

AU - Prescott, Mark

AU - Adler, Ben

AU - Devenish, Rodney

PY - 2011

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AB - Burkholderia pseudomallei, the causal agent of melioidosis, employs a number of virulence factors during its infection of mammalian cells. One such factor is the Type Three Secretion System (TTSS), which is proposed to mediate the transport and secretion of bacterial effector molecules directly into host cells. The B. pseudomallei genome contains three TTSS gene clusters (designated TTSS1, TTSS2 and TTSS3). Previous research has indicated that neither TTSS1 nor TTSS2 are involved in B. pseudomallei virulence in a hamster infection model. We have characterised a B. pseudomallei mutant lacking expression of the predicted TTSS1 ATPase encoded by bpscN. This mutant was significantly attenuated for virulence in a respiratory melioidosis mouse model of infection. In addition, analyses in vitro showed diminished survival and replication in RAW264.7 cells, an increased level of co-localisation with the autophagy marker protein LC3, but an unhindered ability to escape from phagosomes. Taken together, these data provide evidence that the TTSS1 bpscN gene product plays an important role in the intracellular survival of B. pseudomallei and the pathogenesis of murine infection.

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