A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Expression of heterologous O-antigen in Yersinia pestis KIM does not affect virulence by the intravenous route
Tekijät: Oyston PCF, Prior JL, Kiljunen S, Skurnik M, Hill J, Titball RW
Kustantaja: SOC GENERAL MICROBIOLOGY
Julkaisuvuosi: 2003
Lehti:: Journal of Medical Microbiology
Tietokannassa oleva lehden nimi: JOURNAL OF MEDICAL MICROBIOLOGY
Lehden akronyymi: J MED MICROBIOL
Vuosikerta: 52
Numero: 4
Aloitussivu: 289
Lopetussivu: 294
Sivujen määrä: 6
ISSN: 0022-2615
DOI: https://doi.org/10.1099/jmm.0.05044-0
Verkko-osoite: http://jmm.sgmjournals.org/content/52/4/289
Tiivistelmä
All strains of Yersinia pestis examined have been found to lack an O-antigen. In other members, of the Enterobacteriaceae, the rough phenotype often results in attenuation. However, Y. pestis is the aetiological agent of bubonic plague. In evolving from the ancestral enteropathogenic Yersinia pseudo tuberculosis, and with the development of an arthropod-vectored systemic pathogenesis, smooth LIPS production is not necessary for Y. pestis virulence and the metabolic burden has been alleviated by inactivation of the O-antigen biosynthetic operon. To investigate this, Y. pestis strain KIM D27 was transformed with a plasmid carrying the operon encoding the O-antigen of Yersinia enterocolitica O : 3. Expression of the O-antigen could be detected in silver-stained gels. The receptor for bacteriophage phi5YeO3-12 has been shown to be O-antigen, and infection by this bacteriophage results in lysis of Y. enterocolitica O : 3. Expression of the O-antigen in Y. pestis conferred sensitivity to lysis by phi5YeO3-12. The O-antigen-expressing clone was shown to be as virulent in mice by the intravenous route of challenge as the rough wild-type. Assays showed no alteration in the ability of Y. pestis to resist lysis by cationic antimicrobial peptides, serum or polymyxin.
All strains of Yersinia pestis examined have been found to lack an O-antigen. In other members, of the Enterobacteriaceae, the rough phenotype often results in attenuation. However, Y. pestis is the aetiological agent of bubonic plague. In evolving from the ancestral enteropathogenic Yersinia pseudo tuberculosis, and with the development of an arthropod-vectored systemic pathogenesis, smooth LIPS production is not necessary for Y. pestis virulence and the metabolic burden has been alleviated by inactivation of the O-antigen biosynthetic operon. To investigate this, Y. pestis strain KIM D27 was transformed with a plasmid carrying the operon encoding the O-antigen of Yersinia enterocolitica O : 3. Expression of the O-antigen could be detected in silver-stained gels. The receptor for bacteriophage phi5YeO3-12 has been shown to be O-antigen, and infection by this bacteriophage results in lysis of Y. enterocolitica O : 3. Expression of the O-antigen in Y. pestis conferred sensitivity to lysis by phi5YeO3-12. The O-antigen-expressing clone was shown to be as virulent in mice by the intravenous route of challenge as the rough wild-type. Assays showed no alteration in the ability of Y. pestis to resist lysis by cationic antimicrobial peptides, serum or polymyxin.
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