A secreted anti-activator, OspD1, and its chaperone, Spa15, are involved in the control of transcription by the type III secretion apparatus activity in Shigella flexneri.

Bacteria of Shigella spp. are responsible for shigellosis in humans and use a type III secretion (TTS) system to enter epithelial cells and trigger apoptosis in macrophages. Transit of translocator and effector proteins through the TTS apparatus is activated upon contact of bacteria with host cells.

Two msbB genes encoding maximal acylation of lipid A are required for invasive Shigella flexneri to mediate inflammatory rupture and destruction of the intestinal epithelium.

Shigella flexneri is a Gram-negative pathogen that invades and causes inflammatory destruction of the human colonic epithelium, thus leading to bloody diarrhea and dysentery. A type III secretion system that delivers effector proteins into target eukaryotic cells is largely responsible for cell and tissue invasion. However, the respective role of this invasive phenotype and of lipid A, the endotoxin of the Shigella LPS, in eliciting the inflammatory cascade that leads to rupture and destruction of the epithelial barrier, was unknown.

The virulence plasmid pWR100 and the repertoire of proteins secreted by the type III secretion apparatus of Shigella flexneri.

Bacteria of Shigella spp. are the causative agents of shigellosis. The virulence traits of these pathogens include their ability to enter into epithelial cells and induce apoptosis in macrophages.

SopA, the outer membrane protease responsible for polar localization of IcsA in Shigella flexneri.

The spreading ability of Shigella flexneri, a facultative intracellular Gram-negative bacterium, within the host-cell cytoplasm is the result of directional assembly and accumulation of actin filaments at one pole of the bacterium. IcsA/VirG, the 120 kDa outer membrane protein that is required for intracellular motility, is located at the pole of the bacterium where actin polymerization occurs. Bacteria growing in laboratory media and within infected cells release a certain proportion of the surface-exposed IcsA after proteolytic cleavage.

Lack of cleavage of IcsA in Shigella flexneri causes aberrant movement and allows demonstration of a cross-reactive eukaryotic protein.

Once in the cytoplasm of mammalian cells, Shigella flexneri expresses a motile phenotype caused by polar directional assembly of actin. This process depends on accumulation of IcsA (VirG), a 120-kDa protein with ATPase activity, at the pole of the bacterium opposite to that at which ongoing septation occurs. IcsA is also secreted into the bacterial supernatant as a 95-kDa species, after cleavage at an SSRRASS sequence which, when mutagenized, blocks processing.

The unrelated surface proteins ActA of Listeria monocytogenes and IcsA of Shigella flexneri are sufficient to confer actin-based motility on Listeria innocua and Escherichia coli respectively.

Listeria monocytogenes and Shigella flexneri are two unrelated facultative intracellular pathogens which spread from cell to cell by using a similar mode of intracellular movement based on continuous actin assembly at one pole of the bacterium. This process requires the asymmetrical expression of the ActA surface protein in L. monocytogenes and the IcsA (VirG) surface protein in S.

Phosphorylation of IcsA by cAMP-dependent protein kinase and its effect on intracellular spread of Shigella flexneri.

Shigella flexneri, a Gram-negative bacillus belonging to the family Enterobacteriaceae, causes bacillary dysentery in humans by invading colonic epithelial cells. Processes by which epithelial cells, which are not professional phagocytes, may limit the spread of the invading microorganisms are poorly understood. This paper shows that IcsA (VirG), a 120 kDa bacterial outer membrane protein responsible for intracellular and cell-to-cell spread through polymerization of actin, is a major substrate for phosphorylation by cyclic-dependent protein kinases.

OmpB (osmo-regulation) and icsA (cell-to-cell spread) mutants of Shigella flexneri: vaccine candidates and probes to study the pathogenesis of shigellosis.

Genetic and molecular data now available on the pathogenic properties of Shigella flexneri allow rational design of live attenuated vaccine strains. The genes required at given steps of the infection process can be selectively mutated to impair the bacterium's capacity to interact with intestinal epithelial cells and/or survive within intestinal tissues in general. We have tested two mutations in S.

Identification of icsA, a plasmid locus of Shigella flexneri that governs bacterial intra- and intercellular spread through interaction with F-actin.

The capacity of Shigella to spread within the cytosol of infected epithelial cells and to infect adjacent cells is critical for the development of infection foci, which lead to mucosal abscesses. Shigella is a nonmotile microorganism that appears to utilize host cell microfilaments to generate intra- as well as intercellular movements, since this movement was inhibited by cytochalasin D and involvement of F-actin was demonstrated by direct labeling of infected cells with the specific dye N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)phallacidin. Such movements led to the formation of extracellular protrusions, which may explain cell to cell spread.

Detection of enteric pathotypes of Escherichia coli by hybridization using six DNA probes.

A set of 6 DNA probes was tested to evaluate the incidence of various Escherichia coli pathotypes among 540 strains isolated in France from diarrhoeal stools of infants, children and adults. Enterotoxigenic E. coli were detected using 3 gene probes for enterotoxins LT, STaH and STaP.

Presence and expression of aerobactin genes in virulent avian strains of Escherichia coli.

Virulent and nonvirulent isolates of avian Escherichia coli were tested for the presence of aerobactin genes by colony hybridization with a specific gene probe constructed from plasmid pABN1 (A. Bindereif and J. B.

Cloning of plasmid DNA sequences involved in invasion of HeLa cells by Shigella flexneri.

A large plasmid is found in virulent isolates of Shigella sp. and encodes functions essential for invasion of mammalian cells. To identify plasmid sequences necessary for invasion, we isolated a series of Tn5 insertions in pWR100, the virulence plasmid of Shigella flexneri serotype 5.

Epidemiological markers of Shigella sonnei infections: R-plasmid fingerprinting, phage-typing and biotyping.

In 1980, the number of Shigella sonnei strains isolated in Sicily increased markedly. Approximately 80% of the isolates belonged to phage-type 3 and showed the same antibiotic resistance pattern, suggesting that an epidemic had been going on for several months. Plasmid analysis of strains isolated at various times in different places supported this view.

DNA hybridization technique to detect Shigella species and enteroinvasive escherichia coli.

A DNA hybridization method for the detection of Shigella species and enteroinvasive Escherichia coli is described. It is based upon the high degree of homology shared by the virulence plasmids present in all pathogenic strains. After 32P labeling, a 17-kilobase EcoRI restriction fragment of a virulence plasmid belonging to Shigella flexneri serotype 5 was used as a probe to detect Shigella species and enteroinvasive E.

Molecular comparison of virulence plasmids in Shigella and enteroinvasive Escherichia coli.

Virulent isolates of Shigella dysenteriae and Shigella boydii harboured a 140 Mdal plasmid which was either absent or deleted in spontaneously avirulent strains. Together with previous data concerning S. sonnei, S.

Taxonomic value of a chromogenic test for the detection of aminopeptidases in the genus Shigella.

In addition to the conventional methods for the identification of Enterobacteriaceae, enzymatic tests using chromogenic substrates have been proposed [1, 2, 5, 7, 8, 9, 10]. Many chromogenic and fluorogenic substrates are now available, and some of these have been employed for the determination of enzymatic profiles of Neisseria [3] and Enterobacteriaceae [7]. In this article, we report the activity of bacterial cultures of the genus Shigella on a new chromogenic substrate: chromozym PL.

Plasmid-mediated invasiveness of "Shigella-like" Escherichia coli.

Invasive Escherichia coli is a "Shigella-like" microorganism which causes a dysenteric syndrome through invasion of the human colonic epithelium. Representative strains of different serotypes were studied in order to determine whether plasmids are involved in their virulence. All invasive E.

[Fermentation of galacturonate by "Shigella" (author's transl)].

The ability of 300 Shigella strains to produce acid from galacturonate (galacturonate test) was examined. With respect to this galacturonate test, all S. flexnerii serotypes (except serotype 6) were positive, and all S.