The Fim and FhaB adhesins play a crucial role in nasal cavity infection and Bordetella pertussis transmission in a novel mouse catarrhal infection model.
Adenylate Cyclase Toxin
Adhesins, Bacterial
/ metabolism
Animals
Bordetella pertussis
/ genetics
Disease Models, Animal
Humans
Mice
Mice, Inbred C57BL
Myeloid Differentiation Factor 88
Nasal Cavity
/ microbiology
Pertussis Vaccine
Virulence Factors, Bordetella
/ genetics
Whooping Cough
/ transmission
Journal
PLoS pathogens
ISSN: 1553-7374
Titre abrégé: PLoS Pathog
Pays: United States
ID NLM: 101238921
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
received:
17
09
2021
accepted:
28
02
2022
revised:
20
04
2022
pubmed:
9
4
2022
medline:
23
4
2022
entrez:
8
4
2022
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 35395059
doi: 10.1371/journal.ppat.1010402
pii: PPATHOGENS-D-21-01903
pmc: PMC9020735
doi:
Substances chimiques
Adenylate Cyclase Toxin
0
Adhesins, Bacterial
0
Myeloid Differentiation Factor 88
0
Pertussis Vaccine
0
Virulence Factors, Bordetella
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1010402Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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