ArticlePLoS pathogens2020
Cytotoxicity of the effector protein BteA was attenuated in Bordetella pertussis by insertion of an alanine residue.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Revisiting Whooping Cough: Global Drivers and Implications of Pertussis Resurgence in the Acellular Vaccine Era.Vaccines · 2025Review
- An IS element-driven antisense RNA attenuates the expression of serotype 2 fimbriae and the cytotoxicity ofEmerging microbes & infections · 2025Article
- Article
- The Bordetella type III secretion system effector BteA targets host eosinophil-epithelial signaling to promote IL-1Ra expression and persistence.Communications biology · 2025Article
- Limited response of primary nasal epithelial cells toMicrobiology spectrum · 2025Article
- ThemBio · 2024Article
- Eosinophils as drivers of bacterial immunomodulation and persistence.Infection and immunity · 2024Review
- T3SS chaperone of the CesT family is required for secretion of the anti-sigma factor BtrA inEmerging microbes & infections · 2023Article
- Bordetella spp. block eosinophil recruitment to suppress the generation of early mucosal protection.Cell reports · 2023Article
- Review
- BopN is a Gatekeeper of theMicrobiology spectrum · 2023Article
- A comprehensive resource for Bordetella genomic epidemiology and biodiversity studies.Nature communications · 2022Article
- The Fim and FhaB adhesins play a crucial role in nasal cavity infection and Bordetella pertussis transmission in a novel mouse catarrhal infection model.PLoS pathogens · 2022Article
- Conquering the host:Frontiers in microbiology · 2022Review
- Pathogenicity and virulence ofVirulence · 2021Review
- Different roles of conserved tyrosine residues of the acylated domains in folding and activity of RTX toxins.Scientific reports · 2021Article
- Omics Analysis of Blood-Responsive Regulon inInternational journal of molecular sciences · 2021Article
- Adenylate Cyclase Toxin Tinkering With Monocyte-Macrophage Differentiation.Frontiers in immunology · 2020Review
- Review
- Lipid binding by the N-terminal motif mediates plasma membrane localization of Bordetella effector protein BteA.The Journal of biological chemistryArticle
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bordetella bronchiseptica and Bordetella pertussis are closely related respiratory pathogens that evolved from a common bacterial ancestor. While B. bronchiseptica has an environmental reservoir and mostly establishes chronic infections in a broad range of mammals, B. pertussis is a human-specific pathogen causing acute pulmonary pertussis in infants and whooping cough illness in older humans. Both species employ a type III secretion system (T3SS) to inject a cytotoxic BteA effector protein into host cells. However, compared to the high BteA-mediated cytotoxicity of B. bronchiseptica, the cytotoxicity induced by B. pertussis BteA (Bp BteA) appears to be quite low and this has been attributed to the reduced T3SS gene expression in B. pertussis. We show that the presence of an alanine residue inserted at position 503 (A503) of Bp BteA accounts for its strongly attenuated cytotoxic potency. The deletion of A503 from Bp BteA greatly enhanced the cytotoxic activity of B. pertussis B1917 on mammalian HeLa cells and expression of Bp BteAΔA503 was highly toxic to Saccharomyces cerevisiae cells. Vice versa, insertion of A503 into B. bronchiseptica BteA (Bb BteA) strongly decreased its cytotoxicity to yeast and HeLa cells. Moreover, the production of Bp BteAΔA503 increased virulence of B. pertussis B1917 in the mouse model of intranasal infection (reduced LD50) but yielded less inflammatory pathology in infected mouse lungs at sublethal infectious doses. This suggests that A503 insertion in the T3SS effector Bp BteA may represent an evolutionary adaptation that fine-tunes B. pertussis virulence and host immune response.
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