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Chapter 25 : Effector Molecules of Pathogenesis and Host Responses

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Abstract:

This chapter outlines the expression of the invasive phenotype, as well as the effector molecules required and their unique modes of action. The features of the disease involve specific interactions of with different cell populations, particularly intestinal epithelial cells, resident macrophages, and polymorphonuclear leukocytes (PMN). These interactions between invasive bacteria and the host cell initiate diverse responses, leading to rupture, invasion, dissemination, and inflammatory destruction of the intestinal barrier. As a consequence of the development of an acute inflammatory response, the intestinal tissue is destroyed. Therefore, shigellosis is considered to be a disease resulting from an imbalance in the host mechanisms that regulate inflammation in the presence of an invading microorganism. In shigellosis, several lines of evidence indicate that cytokines and chemokines are mediators of tissue damage. It has been shown that several pathogens, such as , , or spp., can induce apoptosis in host Cells. Signals that induce the transmigration of neutrophils are dependent on basolateral membrane- interactions, and require genes encoded by the virulence plasmid as well as a functional type III secretion apparatus. In relation to spp., it will be important (i) to elucidate their human colonic specificity, (ii) to confirm whether bacterial translocation through M cells in vivo is the unique way to invade the colon, (iii) to proceed to exhaustive identification of the signaling pathways that lead to severe inflammation characteristic of shigellosis, and (iv) to improve our understanding regarding the bases of immune protection against the disease.

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25

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Bacterial Proteins
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Bacterial Pathogenesis
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Shigella flexneri
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Figures

Image of FIGURE 1
FIGURE 1

Genetic map of the 30-kg locus or entry region of the 5a virulence plasmid pWR100. On the top, the operon, which encodes the secreted entry effectors, is hatched, and genes that encode for chaperones are indicated in black. At the bottom, the and operons, which encode the type III secretion apparatus components, are shown in gray. The gene codes for the activator required for transcription. Courtesy of C. Parsot (Institut Pasteur, Paris, France).

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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Image of FIGURE 2
FIGURE 2

Ultrastructure of the needle complex of the type III secretion apparatus. (A) Negative staining of the isolated needle complex (arrows) by transmission electron microscopy (courtesy of A. Blocker, P. Gounon, and E. Larquet, Institut Pasteur, Paris, France) and (B and C) representation of the structure of the needle complex. OM and IM, outer and inner bacterial membrane, respectively. Scale bar, 100 nm.

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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Image of FIGURE 3
FIGURE 3

Transmission electron microscopy images of entry into epithelial (HeLa) cells (P. Gounon and P. J. Sansonetti, Institut Pasteur, Paris, France). Note in (A) the formation of cellular extensions on the host cell that will engulf the bacteria. In (B), two bacteria are inside the epithelial cell that shows multiple cellular extensions. Scale bars, 1 m.

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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Image of FIGURE 4
FIGURE 4

Bacterial signals and cell responses during entry. (1) Intracellular IpaC induces actin polymerization by activation of Cdc42 and Rac, and filopodial extensions are formed. (2) Translocated IpaA binds to vinculin, and this complex allows the formation of an adhesive structure at the site of bacterial contact with the host cell membrane. (3) Filopodial extensions are transformed into leaflet structures. (4) Finally, is internalized in a vacuole. Courtesy of G. Tran Van Nhieu (Institut Pasteur, Paris, France).

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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Image of FIGURE 5
FIGURE 5

(A) Actin-dependent motility enables the bacterium to move intracellularly and invade adjacent cells. (B) S1 myosin fragments decorate short actin filaments nucleated, elongated, and assembled at the pole of a bacterium. (C) Bacterium enclosed by a double membrane after invasion of an adjacent cell. (P. Gounon and P. J. Sansonetti, Institut Pasteur, Paris, France.) Scale bars, 1 m.

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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Image of FIGURE 6
FIGURE 6

Model for actin-based movement of . (1) Binding of NWASP to IcsA at surface activates the connector. Arp2/3 is activated and binds to G-actin. (2) Interaction of VCA domain of N-WASP with activated Arp2/3-G-actin complex. (3) The VCA domain shuttles G-actin subunits to the growing barbed end.

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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Image of FIGURE 7
FIGURE 7

Schematic of -induced inflammation: rupture, invasion, and inflammatory destruction of the intestinal barrier.

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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Image of FIGURE 8
FIGURE 8

Signaling pathways in epithelial cells and macrophages induced by infection, LPS, and/or bacterial products.

Citation: Fernandez M, Sansonetti P. 2003. Effector Molecules of Pathogenesis and Host Responses, p 455-480. In Hecht G (ed), Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC. doi: 10.1128/9781555817848.ch25
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