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Nuanced differences in adenylate cyclase toxin production, acylation, and secretion may contribute to the evolution of virulence in Bordetella species
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Nuanced differences in adenylate cyclase toxin production, acylation, and secretion may contribute to the evolution of virulence in Bordetella species
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Nuanced differences in adenylate cyclase toxin production, acylation, and secretion may contribute to the evolution of virulence in Bordetella species
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Journal Article
Nuanced differences in adenylate cyclase toxin production, acylation, and secretion may contribute to the evolution of virulence in Bordetella species
2025
Overview
Bordetella pertussis causes the acute disease whooping cough and survives only in the human respiratory tract, while Bordetella bronchiseptica causes long-term, chronic infections in a broad range of mammals and can also survive in extra-host environments. These bacteria produce a nearly identical set of virulence factors, including adenylate cyclase toxin (ACT), a protein that is modified by the addition of acyl chains. Acylation is required for ACT to cause hemolysis and for efficient intoxication of host cells in vitro . We found that ACT acylation is also important, but not absolutely required, during infection. We also discovered differences in ACT production, acylation, and secretion between B. bronchiseptica and B. pertussis that may contribute to the different virulence strategies of these species. This study highlights the advantage of conducting comparative analyses between closely related species to better understand the evolution of virulence.
Publisher
American Society for Microbiology
Subject
/ Adenylate Cyclase Toxin - genetics
/ Adenylate Cyclase Toxin - metabolism
/ Animals
/ bacterial respiratory infection
/ Bordetella bronchiseptica - genetics
/ Bordetella bronchiseptica - metabolism
/ Bordetella bronchiseptica - pathogenicity
/ Bordetella Infections - microbiology
/ Bordetella pertussis - genetics
/ Bordetella pertussis - metabolism
/ Bordetella pertussis - pathogenicity
/ Humans
/ Mice
/ post-translational modification
/ Proteins
/ Toxins
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