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

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.

Cytotoxicity^a

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 survival^a

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.

Regulation^a

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.