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Infection and immunity2006; 74(12); 6907-6919; doi: 10.1128/IAI.01116-06

Mutation of the maturase lipoprotein attenuates the virulence of Streptococcus equi to a greater extent than does loss of general lipoprotein lipidation.

Abstract: Streptococcus equi is the causative agent of strangles, a prevalent and highly contagious disease of horses. Despite the animal suffering and economic burden associated with strangles, little is known about the molecular basis of S. equi virulence. Here we have investigated the contributions of a specific lipoprotein and the general lipoprotein processing pathway to the abilities of S. equi to colonize equine epithelial tissues in vitro and to cause disease in both a mouse model and the natural host in vivo. Colonization of air interface organ cultures after they were inoculated with a mutant strain deficient in the maturase lipoprotein (DeltaprtM(138-213), with a deletion of nucleotides 138 to 213) was significantly less than that for cultures infected with wild-type S. equi strain 4047 or a mutant strain that was unable to lipidate preprolipoproteins (Deltalgt(190-685)). Moreover, mucus production was significantly greater in both wild-type-infected and Deltalgt(190-685)-infected organ cultures. Both mutants were significantly attenuated compared with the wild-type strain in a mouse model of strangles, although 2 of 30 mice infected with the Deltalgt(190-685) mutant did still exhibit signs of disease. In contrast, only the DeltaprtM(138-213) mutant was significantly attenuated in a pony infection study, with 0 of 5 infected ponies exhibiting pathological signs of strangles compared with 4 of 4 infected with the wild-type and 3 of 5 infected with the Deltalgt(190-685) mutant. We believe that this is the first study to evaluate the contribution of lipoproteins to the virulence of a gram-positive pathogen in its natural host. These data suggest that the PrtM lipoprotein is a potential vaccine candidate, and further investigation of its activity and its substrate(s) are warranted.
Publication Date: 2006-10-02 PubMed ID: 17015455PubMed Central: PMC1698103DOI: 10.1128/IAI.01116-06Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

This research summary has been generated with artificial intelligence and may contain errors and omissions. Refer to the original study to confirm details provided. Submit correction.

The research investigates the role of a specific lipoprotein in the virulence of Streptococcus equi, a bacterium causing a contagious disease in horses, and suggests the lipoprotein as a potential vaccine candidate.

Overview of the Research

  • The research studies the virulence of a bacterium called Streptococcus equi, which causes a prevalent and contagious horse disease, strangles. Specifically, the focus of the study is to explore the contributions of a specific lipoprotein (a protein molecule) and the general lipoprotein processing pathway in the bacterium’s ability to colonize in equine epithelial tissues and cause disease in Equis genus (horse family).

Methodology and Experiments

  • Researchers used organ cultures, a mouse model, and a pony infection study to evaluate the effects of a mutant strain of Streptococcus equi deficient in the maturase lipoprotein (DeltaprtM(138-213)). This involved using a wild-type S. equi strain 4047, and a mutant strain incapable of lipidating preprolipoproteins (Deltalgt(190-685)) for comparative analysis.
  • They examined colonization of air interface organ cultures after inoculation with different strains, and found that colonization was less in those cultures infected with the deficient-maturase strain when compared to ones infected with the wild-type or the non-lipidating strain. They also noted increased mucus production in the wild-type-infected and Deltalgt(190-685)-infected organ cultures.

Findings and Conclusions

  • Both mutant strains were less virulent than the wild-type strain in the mouse model, though there were still instances of disease in those infected with the Deltalgt(190-685) mutant strain.
  • In a pony infection study, only the DeltaprtM(138-213) mutant strain showed significant attenuation, with none of the infected ponies showing signs of strangles disease. Ponies infected with the wild-type strain, and the Deltalgt(190-685) mutant showed prevalent signs of the disease.
  • Based on these results, the study suggests the PrtM maturase lipoprotein as a potential vaccine candidate and encourages further investigation on its activity and substrates.

Cite This Article

APA
Hamilton A, Robinson C, Sutcliffe IC, Slater J, Maskell DJ, Davis-Poynter N, Smith K, Waller A, Harrington DJ. (2006). Mutation of the maturase lipoprotein attenuates the virulence of Streptococcus equi to a greater extent than does loss of general lipoprotein lipidation. Infect Immun, 74(12), 6907-6919. https://doi.org/10.1128/IAI.01116-06

Publication

ISSN: 0019-9567
NlmUniqueID: 0246127
Country: United States
Language: English
Volume: 74
Issue: 12
Pages: 6907-6919

Researcher Affiliations

Hamilton, Andrea
  • University of Sunderland, Tyne and Wear SR1 3SD, United Kingdom.
Robinson, Carl
    Sutcliffe, Iain C
      Slater, Josh
        Maskell, Duncan J
          Davis-Poynter, Nick
            Smith, Ken
              Waller, Andrew
                Harrington, Dean J

                  MeSH Terms

                  • Alleles
                  • Animals
                  • Bacterial Proteins / genetics
                  • Bacterial Vaccines / genetics
                  • Cell Membrane / ultrastructure
                  • Cells, Cultured
                  • Genes, Bacterial
                  • Horse Diseases / immunology
                  • Horse Diseases / microbiology
                  • Horse Diseases / pathology
                  • Horses / immunology
                  • Horses / microbiology
                  • Lipoproteins / metabolism
                  • Mice
                  • Mutation
                  • Peptide Hydrolases / genetics
                  • Streptococcal Infections / microbiology
                  • Streptococcal Infections / pathology
                  • Streptococcal Infections / veterinary
                  • Streptococcus equi / enzymology
                  • Streptococcus equi / genetics
                  • Streptococcus equi / pathogenicity
                  • Vaccines, Attenuated / genetics
                  • Virulence / genetics

                  Grant Funding

                  • Wellcome Trust

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