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BipA Is Associated with Preventing Autoagglutination and Promoting Biofilm Formation in Bordetella holmesii
Yukihiro Hiramatsu1, Momoko Saito2, Nao Otsuka1
1Department of Bacteriology II, National Institute of Infectious Diseases, Tokyo, Japan.
Abstract:
Bordetella holmesii causes both invasive and respiratory diseases in humans. Although the number of cases of pertussis-like respiratory illnesses due to B. holmesii infection has increased in the last decade worldwide, little is known about the virulence factors of the organism. Here, we analyzed a B. holmesii isolate that forms large aggregates and precipitates in suspension, and subsequently demonstrated that the autoagglutinating isolate is deficient in Bordetella intermediate protein A (BipA) and that this deletion is caused by a frame-shift mutation in the bipA gene. A BipA-deficient mutant generated by homologous recombination also exhibited the autoagglutination phenotype. Moreover, the BipA mutant adhered poorly to an abiotic surface and failed to form biofilms, as did two other B. holmesii autoagglutinating strains, ATCC 51541 and ATCC 700053, which exhibit transcriptional down-regulation of bipA gene expression, indicating that autoagglutination indirectly inhibits biofilm formation. In a mouse intranasal infection model, the BipA mutant showed significantly lower levels of initial lung colonization than did the parental strain (P < 0.01), suggesting that BipA might be a critical virulence factor in B. holmesii respiratory infection. Together, our findings suggest that BipA production plays an essential role in preventing autoagglutination and indirectly promoting biofilm formation by B. holmesii.
Insights
Bordetella holmesii autoagglutination is linked to a deficiency in Bordetella intermediate protein A (BipA). Loss of BipA impairs biofilm formation and reduces lung colonization in mice, highlighting BipA
Area of Science:
- Microbiology
- Bacterial Pathogenesis
- Molecular Biology
Background:
- Bordetella holmesii is increasingly recognized for causing respiratory and invasive diseases.
- Understanding B. holmesii virulence factors is crucial due to rising global infections.
- Limited knowledge exists regarding the specific mechanisms of B. holmesii pathogenicity.
Purpose of the Study:
- To investigate the role of Bordetella intermediate protein A (BipA) in B. holmesii autoagglutination.
- To determine the impact of BipA deficiency on biofilm formation and virulence.
- To elucidate the relationship between autoagglutination and biofilm formation in B. holmesii.
Main Methods:
- Analysis of a B. holmesii isolate exhibiting autoagglutination and precipitation.
- Genetic characterization of the bipA gene in autoagglutinating strains.
- Generation of a BipA-deficient mutant using homologous recombination.
- Assessment of bacterial adherence and biofilm formation in vitro.
- Evaluation of lung colonization in a mouse intranasal infection model.
Main Results:
- An autoagglutinating B. holmesii isolate was found to be deficient in BipA due to a frame-shift mutation.
- BipA-deficient mutants exhibited autoagglutination and poor adherence to abiotic surfaces.
- BipA-deficient mutants and other autoagglutinating strains failed to form biofilms.
- Autoagglutination was shown to indirectly inhibit biofilm formation.
- The BipA mutant demonstrated significantly reduced initial lung colonization in mice compared to the parental strain.
Conclusions:
- BipA production is essential for preventing autoagglutination in B. holmesii.
- BipA plays an indirect role in promoting biofilm formation.
- BipA is a critical virulence factor in B. holmesii respiratory infections.
- Deficiency in BipA compromises bacterial colonization and biofilm development.
