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The type III secreted protein BspR regulates the virulence genes in Bordetella bronchiseptica

Jun Kurushima1, Asaomi Kuwae, Akio Abe

  • 1Laboratory of Bacterial Infection, Graduate School of Infection Control Sciences, Kitasato University, Tokyo, Japan.

Plos One
|June 16, 2012
PubMed

Insights

Bordetella bronchiseptica secretes a novel protein, BspR (Bordetella secreted protein regulator), which is crucial for virulence and regulates type III secretion system (T3SS) activity in response to iron levels.

Area of Science:

  • Microbiology
  • Bacterial Pathogenesis
  • Molecular Biology

Background:

  • Bordetella species, including B. bronchiseptica, B. pertussis, and B. parapertussis, are significant human and animal pathogens.
  • The type III secretion system (T3SS) is a key virulence factor in Bordetella, delivering effector proteins into host cells.
  • Identifying novel virulence factors and their regulatory mechanisms is crucial for understanding Bordetella pathogenesis.

Purpose of the Study:

  • To identify novel type III secreted effector proteins in Bordetella bronchiseptica.
  • To characterize the function and regulatory role of a newly identified T3SS effector, designated BspR.
  • To investigate the involvement of BspR in virulence and the regulation of other virulence factors.

Main Methods:

  • Comparative proteomic analysis using iTRAQ to identify secreted proteins in wild-type and T3SS-deficient B. bronchiseptica strains.
  • Construction and phenotypic analysis of a BspR deletion mutant (ΔbspR).
  • Assessment of bacterial virulence using a mouse infection model and evaluation of T3SS-dependent activities (cytotoxicity, hemolysin).

Main Results:

  • BB1639 was identified as a novel type III secreted protein, named BspR (Bordetella secreted protein regulator).
  • A ΔbspR mutant exhibited significantly attenuated virulence in a mouse model and conserved presence in B. pertussis and B. parapertussis.
  • BspR deficiency led to hyper-secretion of T3SS proteins, enhanced cytotoxicity and hemolytic activity, but abolished expression of other key virulence factors (FHA, pertactin, ACT).
  • BspR was found to regulate T3SS in response to iron availability, controlling Bordetella virulence factors coordinately.

Conclusions:

  • BspR is a novel, essential virulence factor and regulator in Bordetella species.
  • BspR plays a critical role in the iron-responsive regulation of the T3SS and other virulence factors.
  • BspR coordinates the inverse regulation of Bordetella virulence factors, impacting pathogenesis.

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