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The Francisella tularensis LVS ΔpdpC mutant exhibits a unique phenotype during intracellular infection

Marie Lindgren, Jeanette E Bröms, Lena Meyer, Igor Golovliov and Anders Sjöstedt*

Author Affiliations

Department of Clinical Microbiology, Clinical Bacteriology and Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå SE-901 85, Sweden

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BMC Microbiology 2013, 13:20  doi:10.1186/1471-2180-13-20

Published: 29 January 2013



A prerequisite for the virulence of the facultative intracellular bacterium Francisella tularensis is effective intramacrophage proliferation, which is preceded by phagosomal escape into the cytosol, and ultimately leads to host cell death. Many components essential for the intracellular life cycle are encoded by a gene cluster, the Francisella pathogenicity island (FPI), constituting a type VI secretion system.


We characterized the FPI mutant ΔpdpC of the live vaccine strain (LVS) of F. tularensis and found that it exhibited lack of intracellular replication, incomplete phagosomal escape, and marked attenuation in the mouse model, however, unlike a phagosomally contained FPI mutant, it triggered secretion of IL-1β, albeit lower than LVS, and markedly induced LDH release.


The phenotype of the ΔpdpC mutant appears to be unique compared to previously described F. tularensis FPI mutants.

Francisella tularensis; Type VI secretion; Cytopathogenicity; Intracellular replication; PdpC