This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Google Scholar
Right arrow Articles by Suar, M.
Right arrow Articles by Hardt, W.-D.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Suar, M.
Right arrow Articles by Hardt, W.-D.

 Previous Article  |  Next Article 

Infection and Immunity, September 2009, p. 3569-3577, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00511-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Accelerated Type III Secretion System 2-Dependent Enteropathogenesis by a Salmonella enterica Serovar Enteritidis PT4/6 Strain{triangledown}

Mrutyunjay Suar,1,{dagger},{ddagger} Balamurugan Periaswamy,1,{dagger} Pascal Songhet,1 Benjamin Misselwitz,1 Andreas Müller,1 Rina Käppeli,1 Marcus Kremer,2 Mathias Heikenwalder,3 and Wolf-Dietrich Hardt1*

Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland,1 Institut für Allgemeine Pathologie und Pathologische Anatomie, Technische Universität München, D-81675 Munich, Germany,2 Institute of Neuropathology, University Hospital of Zurich, CH-8091 Zurich, Switzerland3

Received 7 May 2009/ Returned for modification 1 June 2009/ Accepted 4 June 2009

Salmonella enterica subsp. I serovars Typhimurium and Enteritidis are major causes of enteric disease. The pathomechanism of enteric infection by serovar Typhimurium has been studied in detail. Serovar Typhimurium employs two pathways in parallel for triggering disease, i.e., the "classical" pathway, triggered by type III secretion system 1 (TTSS-1), and the "alternative" pathway, mediated by TTSS-2. It had remained unclear whether these two pathways would also explain the enteropathogenesis of strains from other serovars. We chose the isolate P125109 of the epidemic serovar Enteritidis PT4/6, generated isogenic mutants, and studied their virulence. Using in vitro and in vivo infection experiments, a dendritic cell depletion strategy, and MyD88–/– knockout mice, we found that P125109 employs both the "classical" and "alternative" pathways for triggering mucosal inflammation. The "classical" pathway was phenotypically similar in serovar Typhimurium strain SL1344 and in P125109. However, the kinetics of the "alternative" pathway differed significantly. Via TTSS-2, P125109 colonized the gut tissue more efficiently and triggered mucosal inflammation approximately 1 day faster than SL1344 did. In conclusion, our data demonstrate that different Salmonella spp. can differ in their capacity to trigger mucosal inflammation via the "alternative" pathway in vivo.

* Corresponding author. Mailing address: Institute of Microbiology, D-BIOL, ETH Zürich, Wolfgang-Pauli-Str. 10, CH-8093 Zurich, Switzerland. Phone: 41 44 632 51 43. Fax: 41 44 632 11 29. E-mail: hardt{at}micro.biol.ethz.ch

{triangledown} Published ahead of print on 15 June 2009.

Editor: J. B. Bliska

{dagger} M.S. and B.P. contributed equally to the presented work.

{ddagger} Present address: School of Biotechnology, KIIT University, Bhubaneswar 751024, Orissa, India.

Infection and Immunity, September 2009, p. 3569-3577, Vol. 77, No. 9
0019-9567/09/$08.00+0     doi:10.1128/IAI.00511-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





Copyright © 2010 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»