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

Suar, Mrutyunjay; Periaswamy, Balamurugan; Songhet, Pascal; Misselwitz, Benjamin; Müller, Andreas; Käppeli, Rina; Kremer, Marcus; Heikenwalder, Mathias; Hardt, Wolf-Dietrich

doi:10.1128/iai.00511-09

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Journal article

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

Suar, Mrutyunjay Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland
Periaswamy, Balamurugan Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland
Songhet, Pascal Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland
Misselwitz, Benjamin Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland
Müller, Andreas Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland
Käppeli, Rina Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland
Kremer, Marcus Institut für Allgemeine Pathologie und Pathologische Anatomie, Technische Universität München, D-81675 Munich, Germany
Heikenwalder, Mathias Institute of Neuropathology, University Hospital of Zurich, CH-8091 Zurich, Switzerland
Hardt, Wolf-Dietrich Institute of Microbiology, D-BIOL, ETH Zürich, CH-8093 Zurich, Switzerland

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Infection and Immunity. - American Society for Microbiology. - 2009, vol. 77, no. 9, p. 3569-3577

English ABSTRACT

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.

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