The virulence protein PagN contributes to the advent of a hyper-replicating cytosolic bacterial population.

subspecies serovar Typhimurium is an intracellular pathogen that invades and colonizes the intestinal epithelium. Following bacterial invasion, is enclosed within a membrane-bound vacuole known as a -containing vacuole (SCV). However, a subset of has the capability to prematurely rupture the SCV and escape, resulting in hyper-replication within the cytosol of epithelial cells.

Differential Salmonella Typhimurium intracellular replication and host cell responses in caecal and ileal organoids derived from chicken.

Chicken infection with Salmonella Typhimurium is an important source of foodborne human diseases. Salmonella colonizes the avian intestinal tract and more particularly the caecum, without causing symptoms. This thus poses a challenge for the prevention of foodborne transmission.

Epithelial cell invasion by typhimurium induces modulation of genes controlled by aryl hydrocarbon receptor signaling and involved in extracellular matrix biogenesis.

is the only bacterium able to enter a host cell by the two known mechanisms: trigger and zipper. The trigger mechanism relies on the injection of bacterial effectors into the host cell through the type III secretion system 1. In the zipper mechanism, mediated by the invasins Rck and PagN, the bacterium takes advantage of a cellular receptor for invasion.

Two In Vivo Models to Study Salmonella Asymptomatic Carrier State in Chicks.

In chicken, Salmonella Enteritidis and Salmonella Typhimurium, the two main serotypes isolated in human infections, can persist in the host organism for many weeks and up to many years without causing any symptoms. This persistence generally occurs after a short systemic infection that may either lead to death of very young birds or develop into cecal asymptomatic persistence, which is often accompanied by a high level of bacterial excretion, facilitating Salmonella transmission to counterparts. Here we describe two models of chick infection.

Murine AML12 hepatocytes allow Salmonella Typhimurium T3SS1-independent invasion and intracellular fate.

Numerous studies have demonstrated the key role of the Salmonella Pathogenicity Island 1-encoded type III secretion system (T3SS1) apparatus as well as its associated effectors in the invasion and intracellular fate of Salmonella in the host cell. Several T3SS1 effectors work together to control cytoskeleton networks and induce massive membrane ruffles, allowing pathogen internalization. Salmonella resides in a vacuole whose maturation requires that the activity of T3SS1 subverts early stages of cell signaling.