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Table 2 Description of pathogenic mechanisms of action included in DBSecSys 2.0

From: DBSecSys 2.0: a database of Burkholderia mallei and Burkholderia pseudomallei secretion systems

Name Pathogens use this mechanism to:
Actin cytoskeleton rearrangement Subvert the host cell cytoskeleton to promote attachment to the host cell surface, internalization in the host cell, and prevent uptake by phagocytic cells.
Actin-based motility Bind to host actin, triggering actin polymerization on the pathogens’ surface and producing a mechanical force that propels them through the host cell and facilitates cell-to-cell spread.
Adhesion Attach to the host cell surface, promoting bacterial internalization in the host cell.
Apoptosis Exert control on the processes that regulate apoptosis in the host.
Cytotoxicitya Secrete toxins into the host cell.
Interference with signaling Interfere with the host signaling cascade, promoting their internalization in the host cell and intracellular survival.
Interference with the immune response Downregulate host inflammatory responses, promoting their internalization in the host cell and intracellular survival.
Intracellular survivala Evade the host immune response and multiply in the host cell.
Invasion Promote their ability to invade the host cell.
Multinucleated giant cell formation Induce host cell fusion and multinucleated giant cell formation.
Phagosomal escape and evasion of autophagy Ensure bacterial escape from endocytic vesicles as well as to evade autophagosomes, ensuring the pathogens’ intracellular survival and cell-to-cell spread.
Regulationa Control secretion system activation and related mechanisms of pathogenicity.
Ubiquitination–deubiquitination Interfere with host ubiquitination processes to attenuate the host immune response, to prevent their degradation, and to ensure their destruction when no longer required for establishing the infection.
  1. aMechanisms of action added in the updated database