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Abstract
The classical bordetellae possess several partially characterized virulence
mechanisms that are studied in the context of a complete extracellular life cycle in their
mammalian host. Yet, classical bordetellae have repeatedly been reported within dendritic
cells and alveolar macrophages in clinical samples, and in vitro experiments convincingly
demonstrate that the bacteria can survive intracellularly within mammalian phagocytic
cells, an ability that appears to have descended from ancestral progenitor species that lived
in the environment and acquired the mechanisms to resist unicellular phagocytic predator.
Many pathogens, including Mycobacterium tuberculosis, Salmonella enterica, Francisella
tularensis, and Legionella pneumophila are known to parasitize and multiply inside
eukaryotic host cells. This strategy provides protection, nutrients, and the ability to
disseminate systemically. While some work has been dedicated at characterizing
B. pertussis intracellular survival phenotype, there is very little understanding of how this
strategy has evolved within the genus Bordetella and contributes to bacterial pathogenicity,
evasion of host immunity and systemic dissemination. Here, we explore the mechanisms
that control the changes accompanying intracellular survival and how these have been
acquired and conserved throughout the divergent evolutionary histories of Bordetella
species.
mechanisms that are studied in the context of a complete extracellular life cycle in their
mammalian host. Yet, classical bordetellae have repeatedly been reported within dendritic
cells and alveolar macrophages in clinical samples, and in vitro experiments convincingly
demonstrate that the bacteria can survive intracellularly within mammalian phagocytic
cells, an ability that appears to have descended from ancestral progenitor species that lived
in the environment and acquired the mechanisms to resist unicellular phagocytic predator.
Many pathogens, including Mycobacterium tuberculosis, Salmonella enterica, Francisella
tularensis, and Legionella pneumophila are known to parasitize and multiply inside
eukaryotic host cells. This strategy provides protection, nutrients, and the ability to
disseminate systemically. While some work has been dedicated at characterizing
B. pertussis intracellular survival phenotype, there is very little understanding of how this
strategy has evolved within the genus Bordetella and contributes to bacterial pathogenicity,
evasion of host immunity and systemic dissemination. Here, we explore the mechanisms
that control the changes accompanying intracellular survival and how these have been
acquired and conserved throughout the divergent evolutionary histories of Bordetella
species.