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Chapter 12 : Molecular Pathogenesis of Enteropathogenic

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Abstract:

can cause gastrointestinal disease by a variety of mechanisms. This chapter focuses on the molecular pathogenesis of one specific category of diarrheagenic , the enteropathogenic (EPEC). It discusses the various bacterial factors and genes involved in EPEC pathogenesis as well as the specific changes that occur in the host cell in response to EPEC infection. Some studies report that the ability of EPEC to enter cell cultures exceeds that of Enteroinvasive (EIEC), but other investigators argue that the methodology of some invasion assays gives artificially elevated invasion levels for strongly adherent bacteria such as EPEC. As for many other bacterial pathogens, expression of EPEC virulence factors is regulated by a trans-acting regulator. The lack of tropomyosin accumulation with EPEC compared with the accumulation with suggests that the cytoskeletal rearrangement caused by EPEC forms a relatively inert, stable cytoskeletal structure that the bacterium rests on but does not promote an actin-myosin-tropomyosin-mediated event involved in mechanical bacterial uptake. Activation of protein kinase C induces rapid changes in intestinal water and electrolyte secretion in vivo and in vitro, thereby suggesting another possible intracellular mediator of the secretory response to EPEC infection. Several EPEC mutants were examined for their abilities to induce phosphorylation of Hp90. A strain cured of the 60-MDa plasmid encoding bundle-forming pilus (BFP) could still phosphorylate Hp90.

Citation: Kaper J. 1994. Molecular Pathogenesis of Enteropathogenic , p 173-195. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch12
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Figure 1

Attaching and effacing of intestinal epithelial cells from a gnotobiotic pig infected with EPEC. The inset is an enlargement of the box in the main part of the figure. Taken from Moon et al. ( ).

Citation: Kaper J. 1994. Molecular Pathogenesis of Enteropathogenic , p 173-195. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch12
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Image of Figure 2
Figure 2

A three-stage model of EPEC pathogenesis ( ). In the first stage (A), nonintimate adherence between the bacterium and the epithelial cells is mediated by the bundle-forming pilus (BFP) and probably other fimbriae. The structural gene is encoded on a large plasmid, and at least one additional gene required for formation of an active bundle-forming pilus is encoded on the chromosome In the second stage (B), a signal transduction event results in increased intracellular calcium levels, release of inositol phosphates, tyrosine phosphorylation of a 90-kDa epithelial cell protein (Hp90), and effacement of microvilli. Chromosomal genes encode a specialized protein secretion pathway which presumably allows presentation of the bacterial products triggering the signal transduction event. A plasmid-encoded regulator encoded by the locus activates transcription of and other genes in the regulon. In the third stage (C), intimate adherence of the bacterium to the epithelium is mediated by intimin (solid triangle), a 94-kDa outer membrane protein encoded by the locus. The intimate adherence of the bacterium amplifies the accumulation of filamentous actin and other cytoskeletal proteins (other geometric shapes) within the epithelial cell.

Citation: Kaper J. 1994. Molecular Pathogenesis of Enteropathogenic , p 173-195. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch12
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Figure 3

Loss of intimate adherence owing to mutation of the gene. (A) Intimate adherence of parent strain E2348/69 to Caco-2 cells. (B) Nonintimate adherence of isogenic deletion mutant CVD206. Taken from Donnenberg and Kaper ( ).

Citation: Kaper J. 1994. Molecular Pathogenesis of Enteropathogenic , p 173-195. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch12
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Figure 4

Alignment of predicted sequences of EPEC intimin and invasin ( ). Sequences are displayed from the N terminus (left) to the С terminus by using the program PlotSimilarity from the Genetics Computer Group, Inc., Madison, Wis. The identity score is shown on the left axis, and the dashed line across the entire length of the proteins denotes the average identity between the proteins.

Citation: Kaper J. 1994. Molecular Pathogenesis of Enteropathogenic , p 173-195. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch12
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Figure 5

Alignment of predicted sequences of EPEC and EHEC intimins ( ) arranged as described in the legend to Fig. 4.

Citation: Kaper J. 1994. Molecular Pathogenesis of Enteropathogenic , p 173-195. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch12
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