Images

  • Colonies of a virulent mutant of Shigella flexneri grown onto a congo red plate
  • Transmission electron microscopy image showing S. flexneri 5a localized close to microvilli of the apical side of intestinal epithelial cells
  • Genetic map of pWR100
  • Structural analysis of the S. flexneri TTS apparatus and needle complex by electron microscopy
  • Model of the regulatory cascade controlling ipaH transcription in response to two external signals
  • Scanning electron micrograph of an epithelial cell internalising a bacteria
  • Model of entry of Shigella in epithelial cells
  • Immunofluorescence staining of a cell infected by Shigella
  • Histology of a human colon infected by Shigella with a massive recruitment of polymorphoclear neutrophiles inducing a rupture of the epithelial barrier
  • Invasion steps of the intestinal epithlelium by Shigella
  • EM picture of a polymorphonuclear neutrophile that has internalised bacteria
  • Picture of a membrane spotted with PCR products of genes involved in inflammation
  • Image of part of the lung obtained by Magnetic Resonance Imaging on a mouse infected by Klebsiella pneumoniae.
  • Digital autoradiograms obtained with a Micro-imager of lungs from mice injected with recombinant Secretory Component-IgAC5 labeled with [35S]-cysteine
  • Endocytosed LPS in m-ICcl2 cells triggers NF-kB translocation

Colonies of a virulent mutant of Shigella flexneri grown onto a congo red plate

Transmission electron microscopy image showing S. flexneri 5a localized close to microvilli of the apical side of intestinal epithelial cells

Genetic map of pWR100

The position and direction of transcription of the various genes and ORFs are indicated by arrows. ORFs for which no function could be proposed are labelled according to their coordinates (in kb) on the sequence. Genes truncated or inactivated by frameshifts are indicated in parenthesis. The colours refer to the G+C content of each ORF: red, <40%; blue, between 40 and 50%; green, >50%. The position of IS sequences is indicated by yellow bars.

Structural analysis of the S. flexneri TTS apparatus and needle complex by electron microscopy

A: Negative staining of one TTS apparatus on osmotically shocked bacteria. B: Deduced projection density map of an averaging of images as shown in A. C: Negative staining of one purified needle complex. D: Average image of a set of purified needle complexes. E: Surface representation of the volume of the needle complex, assuming cylindrical symmetry. This figure was designed by Eric Larquet and Pierre Gounon (Station Centrale de Microscopie Electronique, Institut Pasteur, Paris) and used materials presented in Blocker et al. (1999, 2000).

Model of the regulatory cascade controlling ipaH transcription in response to two external signals

Only the relevant genes are presented on a schematic map of the virulence plasmid. Panel A: in response to a shift in temperature to 37ƒC (1), the virF gene is transcribed and VirF activates the virB promoter (2). VirB activates, directly or indirectly, transcription of genes of the entry region (3), including mxiE and the mxi and spa operons (not detailed) and the ipgC, ipaB, and ipaC genes. The Mxi-Spa apparatus is assembled in the bacterial envelope (4), in an inactive form (dashed square). IpaB and IpaC independently associate with IpgC (5) and MxiE is not active. Panel B: in response to an external signal such as contact with eukaryotic cells (6), the Mxi-Spa apparatus is activated (open square) (7) and IpaB and IpaC are secreted and associate in the extracellular milieu (8). Secretion of IpaB and IpaC results in the presence of free IpgC (9) that interacts, possibly transiently, with MxiE (10) to render it able to activate the ipaH promoter (11) and other regulated promoters (not shown). Products of regulated genes, such as IpaH, are secreted (12).

Scanning electron micrograph of an epithelial cell internalising a bacteria

The cell makes membrane ruffles that engulf the bacteria and internalised it.

Model of entry of Shigella in epithelial cells

Upon contact with an epithelial cell, Shigella injects proteins into the host cell cytoplasm. IpaC activates Cdc42/Rac and c-srs, which induce actin polymerisation required for membrane ruffles formation. C-srs activates as well p190RhoGAP, which decreases Rho activity, leading, together with the IpaA-vinculin complex, to actin depolymerisation at a later stage of the entry.

Immunofluorescence staining of a cell infected by Shigella

Actin is labeled in green and bacteria in red.

Histology of a human colon infected by Shigella with a massive recruitment of polymorphoclear neutrophiles inducing a rupture of the epithelial barrier

Invasion steps of the intestinal epithlelium by Shigella

Shigella first enters the intestinal epithelium via M cells. After lysis of the phagocitic vacuole, Shigella exists M cells and enters underlying macrophages and kill them by apoptosis. It then induces its entry into epithelial cells by the baso-lateral side, lyses the phagocitic membranes, and by using actin-based motility, spread from one cell to the other.

EM picture of a polymorphonuclear neutrophile that has internalised bacteria

Picture of a membrane spotted with PCR products of genes involved in inflammation

Image of part of the lung obtained by Magnetic Resonance Imaging on a mouse infected by Klebsiella pneumoniae.

The signal in the lungs is increased due to the infection.

Digital autoradiograms obtained with a Micro-imager of lungs from mice injected with recombinant Secretory Component-IgAC5 labeled with [35S]-cysteine

Endocytosed LPS in m-ICcl2 cells triggers NF-kB translocation

S. flexneri 5a LPS (in blue, arrow) internalized in m-ICcl2 polarized epithelial cells after 2 hr of incubation induces NF-kB p65 subunit (in red) translocation from the cytoplasm to the nucleus, which appears as a strong red colour.

Updated on 07/04/2014

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