ArticlePLoS pathogens2022
The Fim and FhaB adhesins play a crucial role in nasal cavity infection and Bordetella pertussis transmission in a novel mouse catarrhal infection model.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- C-terminal domain of the filamentous hemagglutinin FhaB is crucial for interaction ofbioRxiv : the preprint server for biology · 2026Article
- Released palmitic acid-mediated TLR4/NF-κB activation enhances the virulence of Bordetella pertussis MT28 lineage.Nature communications · 2026Article
- Bacteria deliver a microtubule-binding protein into mammalian cells to promote colonization.Science (New York, N.Y.) · 2026Article
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- Genomic surveillance reveals global spread of macrolide-resistantJournal of clinical microbiology · 2025Article
- Innovative adjuvant strategies for next-generation pertussis vaccines.Human vaccines & immunotherapeutics · 2025Review
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- Molecular Epidemiology and Antibiotic Resistance Associated withMicroorganisms · 2025Article
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- Metabolically-versatile Ca. Thiodiazotropha symbionts of the deep-sea lucinid clamISME communications · 2024Article
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- Generating enhanced mucosal immunity againstFrontiers in immunology · 2023Article
- Interference of flagellar rotation up-regulates the expression of small RNA contributing toScience advances · 2022Article
- Evaluation of Whole-Cell and Acellular Pertussis Vaccines in the Context of Long-Term Herd Immunity.Vaccines · 2022Review
- Modeling the catarrhal stage of Bordetella pertussis upper respiratory tract infections in mice.Disease models & mechanisms · 2022Article
- Conquering the host:Frontiers in microbiology · 2022Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary infections caused by Bordetella pertussis used to be the prime cause of infant mortality in the pre-vaccine era and mouse models of pertussis pneumonia served in characterization of B. pertussis virulence mechanisms. However, the biologically most relevant catarrhal disease stage and B. pertussis transmission has not been adequately reproduced in adult mice due to limited proliferation of the human-adapted pathogen on murine nasopharyngeal mucosa. We used immunodeficient C57BL/6J MyD88 KO mice to achieve B. pertussis proliferation to human-like high counts of 108 viable bacteria per nasal cavity to elicit rhinosinusitis accompanied by robust shedding and transmission of B. pertussis bacteria to adult co-housed MyD88 KO mice. Experiments with a comprehensive set of B. pertussis mutants revealed that pertussis toxin, adenylate cyclase toxin-hemolysin, the T3SS effector BteA/BopC and several other known virulence factors were dispensable for nasal cavity infection and B. pertussis transmission in the immunocompromised MyD88 KO mice. In contrast, mutants lacking the filamentous hemagglutinin (FhaB) or fimbriae (Fim) adhesins infected the nasal cavity poorly, shed at low levels and failed to productively infect co-housed MyD88 KO or C57BL/6J mice. FhaB and fimbriae thus appear to play a critical role in B. pertussis transmission. The here-described novel murine model of B. pertussis-induced nasal catarrh opens the way to genetic dissection of host mechanisms involved in B. pertussis shedding and to validation of key bacterial transmission factors that ought to be targeted by future pertussis vaccines.
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