Abstract
BackgroundEnteropathogenic Escherichia coli (EPEC) is an attaching and effacing (A/E) pathogen that possesses a type III secretion system (T3SS) encoded within the locus of enterocyte effacement (LEE). The LEE is essential for A/E lesion formation and directs the secretion and translocation of multiple LEE-encoded and non-LEE encoded effector proteins into the cytosol of infected cells. In this study we used proteomics to compare proteins exported to the culture supernatant by wild type EPEC E2348/69, a ΔespADB mutant and a ΔescF T3SS mutant.ResultsWe observed that flagellin was consistently and strongly present in the secretome of wild type EPEC and the ΔespADB mutant but present only weakly in the secretome of the ΔescF mutant. Given the ancestral relationship between the flagella export apparatus and virulence associated T3SSs, we investigated whether FliC could utilise the LEE-encoded T3SS for export. In the absence of a functional flagella export apparatus, we showed that FliC could be secreted by the LEE-encoded T3SS and stimulate (Toll-like receptor 5) TLR5 signalling but could not confer motility.ConclusionSince the secretion of FliC during A/E lesion formation would presumably be disadvantageous for the pathogen, we propose that virulence associated T3SSs and flagella T3SSs have evolved through a system of chaperones and complex regulatory pathways to be functional at different times to ensure that FliC secretion does not occur during T3SS effector translocation.
Highlights
Enteropathogenic Escherichia coli (EPEC) is an attaching and effacing (A/E) pathogen that possesses a type III secretion system (T3SS) encoded within the locus of enterocyte effacement (LEE)
Both the ΔespADB mutant and ICC171 were grown in HEPES buffered DMEM pH 7.4–7.7 to an OD600 of 1.0 to induce expression of the LEE T3SS
We did not identify any non-LEE encoded effector proteins using this approach, we did find that FliC was present abundantly in the supernatants of the ΔespADB mutant (Fig. 1) and wild-type EPEC but was greatly reduced in the supernatant of the ΔescF mutant, ICC171 (Fig. 1)
Summary
Enteropathogenic Escherichia coli (EPEC) is an attaching and effacing (A/E) pathogen that possesses a type III secretion system (T3SS) encoded within the locus of enterocyte effacement (LEE). The LEE is essential for A/E lesion formation and directs the secretion and translocation of multiple LEE-encoded and non-LEE encoded effector proteins into the cytosol of infected cells. A/E lesion formation is mediated by proteins encoded within a large pathogenicity island called the locus of enterocyte effacement (LEE) [5], which is essential for A/E lesion formation and highly conserved among (page number not for citation purposes). The T3SS secretes and translocates virulence effector proteins from the bacterial cytosol directly into the host cell cytoplasm, where the effector proteins facilitate disease development [10]. Despite the architectural similarity between the flagella biosynthesis machinery and T3SSs, the structural components of the needle complex share limited sequence similarity with components of the flagella basal body [12,13]
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