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Large plasmids associated with virulence in Shigella species have a common function necessary for epithelial cell
Infection and Immunity
|April 1, 1985
Abstract:
Large plasmids (120 to 140 megadaltons) associated with virulence of Shigella sonnei, S. flexneri 2a and S. dysenteriae 1 were transferred from each strain into Escherichia coli K-12 and avirulent S. flexneri 1b strains by ampicillin transposon (Tn1)-mediated conduction. Strains with the virulence plasmid could penetrate tissue culture cells irrespective of the original host of the plasmid.
Insights
Large virulence plasmids from Shigella species were transferred into Escherichia coli. These plasmids enabled bacterial invasion of tissue culture cells, regardless of the host.
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Shigella species are major causes of bacterial dysentery.
- Virulence in Shigella is often mediated by large plasmids.
- Understanding plasmid-mediated virulence is crucial for controlling Shigella infections.
Purpose of the Study:
- To investigate the role of large virulence plasmids in Shigella species.
- To determine if these plasmids confer invasive properties to non-pathogenic bacteria.
Main Methods:
- Conjugal transfer of large plasmids (120-140 megadaltons) from virulent Shigella sonnei, S. flexneri 2a, and S. dysenteriae 1 strains.
- Transfer was mediated by ampicillin transposon (Tn1).
- Recipient strains included Escherichia coli K-12 and avirulent S. flexneri 1b.
Main Results:
- Transposon-mediated conjugation successfully transferred large virulence plasmids.
- Escherichia coli and avirulent S. flexneri strains harboring Shigella virulence plasmids gained the ability to penetrate tissue culture cells.
- Invasiveness was independent of the plasmid's original host strain.
Conclusions:
- Large plasmids carrying virulence factors are transferable between bacterial species.
- These plasmids are sufficient to confer invasive phenotype on recipient bacteria.
- Plasmid-mediated invasion is a key mechanism in Shigella pathogenesis.