ArticlePloS one2016
BipA Is Associated with Preventing Autoagglutination and Promoting Biofilm Formation in Bordetella holmesii.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Role of Tad pili during the transition from planktonic to biofilm state inJournal of bacteriology · 2026Article
- Article
- Novel rRNA transcriptional activity of NhaR revealed by its growth recovery for theFrontiers in molecular biosciences · 2023Article
- Cyclic di-GMP Regulates the Type III Secretion System and Virulence in Bordetella bronchiseptica.Infection and immunity · 2022Article
- In vivo evolution of an emerging zoonotic bacterial pathogen in an immunocompromised human host.Nature communications · 2021Article
- BipA exerts temperature-dependent translational control of biofilm-associated colony morphology ineLife · 2021Article
- Response ofPeerJ · 2021Article
- Hik36-Hik43 and Rre6 act as a two-component regulatory system to control cell aggregation in Synechocystis sp. PCC6803.Scientific reports · 2020Article
- Bacterial autoaggregation.AIMS microbiology · 2018Review
- Bordetella holmesii: Lipid A Structures and Corresponding Genomic Sequences Comparison in Three Clinical Isolates and the Reference Strain ATCC 51541.International journal of molecular sciences · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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