A translocation-competent pore is required for to escape from the double membrane vacuole during intercellular spread.

Unlabelled: Type 3 secretion systems (T3SSs) enable bacterial virulence by translocating virulence proteins (effectors) into host cells. require T3SS to invade and to spread between cells in the colon. In order to spread, forms membrane protrusions that push into the adjacent host cell.

Topology and Contribution to the Pore Channel Lining of Plasma Membrane-Embedded Shigella flexneri Type 3 Secretion Translocase IpaB.

spp. are human bacterial pathogens that cause bacillary dysentery. Virulence depends on a type 3 secretion system (T3SS), a highly conserved structure present in multiple important human and plant pathogens.

The type 3 secretion system requires actin polymerization to open translocon pores.

Many bacterial pathogens require a type 3 secretion system (T3SS) to establish a niche. Host contact activates bacterial T3SS assembly of a translocon pore in the host plasma membrane. Following pore formation, the T3SS docks onto the translocon pore.

Coronavirus Disease 2019 in a Patient With a Systemic Autoinflammatory Syndrome due to an NLRC4 Inflammasomopathy.

The effect of autoinflammatory diseases on severe acute respiratory syndrome coronavirus 2 infection remains unknown. We report a case of coronavirus disease 2019 (COVID-19) in a patient with autoinflammation with infantile enterocolitis with inflammatory flares due to a mutation in the inflammasome component NLRC4. This case highlights the role of immunosuppression in patients with autoinflammation with COVID-19.

Shigella flexneri Disruption of Cellular Tension Promotes Intercellular Spread.

During infection, some bacterial pathogens invade the eukaryotic cytosol and spread between cells of an epithelial monolayer. Intercellular spread occurs when these pathogens push against the plasma membrane, forming protrusions that are engulfed by adjacent cells. Here, we show that IpaC, a Shigella flexneri type 3 secretion system protein, binds the host cell-adhesion protein β-catenin and facilitates efficient protrusion formation.