B. C. Russo

Vimentin regulates mitochondrial ROS production and inflammatory responses of neutrophils

This study shows vimentin regulates neutrophil mitochondrial ROS production and inflammatory responses by modulating mitochondrial function and ROS levels.

Synaptopodin is required for efficient intercellular spread by bacterial pathogens

This study identifies synaptopodin as essential for efficient intercellular spread of Shigella flexneri and Listeria monocytogenes by stabilizing actin tails and enabling protrusion formation.

Longitudinal characterization of circulating neutrophils uncovers distinct phenotypes associated with disease severity in hospitalized COVID-19 patients

This study identifies distinct neutrophil phenotypes linked to disease severity in hospitalized COVID-19 patients using longitudinal data and multi-omics analyses.

Topology and contribution to the pore channel lining of plasma membrane-embedded S. flexneri type 3 secretion translocase IpaB

The paper maps the topology of IpaB in Shigella translocons and shows its role in forming the pore channel for virulence protein delivery.

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

This study shows actin polymerization is required for T3SS translocon pore opening, enabling effector translocation, but not for docking or membrane insertion.

Shigella flexneri disruption of host cell-cell tension promotes intercellular spread

This study shows that Shigella flexneri uses IpaC to reduce cell-cell tension, enabling intercellular spread by forming protrusions.

Activation of Shigella flexneri type 3 secretion requires a host-induced conformational change to the translocon pore

This paper shows that host intermediate filaments induce conformational changes in the Shigella T3SS pore, enabling docking and effector secretion.

Topological analysis of the type 3 secretion system translocon pore protein IpaC following its native delivery to the plasma membrane during infection

The paper determines the topology of IpaC and SipC translocon pore proteins in their native context during infection, resolving conflicting data and identifying topological differences that may underlie functional divergence.