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Journal of Bacteriology, November 2009, p. 6918-6927, Vol. 191, No. 22
0021-9193/09/$08.00+0     doi:10.1128/JB.00532-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Thioredoxin 1 Participates in the Activity of the Salmonella enterica Serovar Typhimurium Pathogenicity Island 2 Type III Secretion System {triangledown}

Aurel Negrea,1 Eva Bjur,2 Speranta Puiac,1 Sofia Eriksson Ygberg,3 Fredrik Åslund,4 and Mikael Rhen1*

Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm 17177, Sweden,1 McGill University, Department of Microbiology and Immunology, Montreal H3A2B4, Canada,2 Swedish Center for Infectious Disease Control, Solna 17182, Sweden,3 European Patent Office, The Hague 2288, The Netherlands4

Received 21 April 2009/ Accepted 10 September 2009

The facultative intracellular pathogen Salmonella enterica serovar Typhimurium relies on its Salmonella pathogenicity island 2 (SPI2) type III secretion system (T3SS) for intracellular replication and virulence. We report that the oxidoreductase thioredoxin 1 (TrxA) and SPI2 are coinduced for expression under in vitro conditions that mimic an intravacuolar environment, that TrxA is needed for proper SPI2 activity under these conditions, and that TrxA is indispensable for SPI2 activity in both phagocytic and epithelial cells. Infection experiments in mice demonstrated that SPI2 strongly contributed to virulence in a TrxA-proficient background whereas SPI2 did not affect virulence in a trxA mutant. Complementation analyses using wild-type trxA or a genetically engineered trxA coding for noncatalytic TrxA showed that the catalytic activity of TrxA is essential for SPI2 activity in phagocytic cells whereas a noncatalytic variant of TrxA partially sustained SPI2 activity in epithelial cells and virulence in mice. These results show that TrxA is needed for the intracellular induction of SPI2 and provide new insights into the functional integration between catalytic and noncatalytic activities of TrxA and a bacterial T3SS in different settings of intracellular infections.

* Corresponding author. Mailing address: Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm 17177, Sweden. Phone: 46-8-524 8 6252. Fax: 46-8-330498. E-mail: mikael.rhen{at}ki.se

{triangledown} Published ahead of print on 18 September 2009.

Journal of Bacteriology, November 2009, p. 6918-6927, Vol. 191, No. 22
0021-9193/09/$08.00+0     doi:10.1128/JB.00532-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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