Skip to main content

Currently Skimming:

Exploitation of Host Cells by Enteropathogenic Escherichia coli
Pages 48-55

The Chapter Skim interface presents what we've algorithmically identified as the most significant single chunk of text within every page in the chapter.
Select key terms on the right to highlight them within pages of the chapter.


From page 48...
... is an extracellular pathogen that causes disease by binding to the surface of host cells and directly injecting virulence factors into the underlying cell through its type III secretion system (2~. These translocated bacterial proteins then interact with host cell components and alter signaling pathways, resulting in disease.
From page 49...
... The type III secretion machinery is thought to generate a pore permitting this translocation to occur (2, 54. Type III secretion systems also play an important role during infection by other Gram-negative pathogenic bacteria such as Yersinia and Salmonella, enabling virulence factors to be translocated directly from the bacterial cytoplasm to the host-cell membrane or cytoplasm.
From page 50...
... Intimate Adherence and the Role of Tir The third stage of EPEC infection is characterized by enterocyte effacement, pedestal formation, and intimate bacterial attachment to the host cell. Intimate attachment requires the outer bacterial membrane protein, intimin.
From page 51...
... Signal Transduction Another critical form of cellular exploitation used by EPEC involves the subversion of host signaling pathways to aid in infection. As a result, several signal transduction pathways are stimulated within epithelial cells after EPEC infection.
From page 52...
... The diarrhea seen during EPEC infection could be caused by the dramatic loss of absorptive microvilli in the A/E lesion (3~. Alternatively, at least one study has shown that EPEC infection reduces the tight junction integrity of epithelial cell monolayers, based on altered distribution of tight junction proteins such as zone occludens (ZO)
From page 53...
... As a result, intestinal epithelial cells have evolved selective physical, chemical, and immunological barriers that permit this mutually beneficial co-existence (51~. Not surprisingly, studies using epithelial cell cultures can only model the intestinal epithelium in a limited fashion.
From page 54...
... With our present knowledge of the factors that mediate bacterial adhesion to the host cell, and the demonstration that preventing bacterial adherence prevents most aspects of the disease, we have already identified potential targets for vaccination. Although the pathogenic effects of A/E lesion formation still need to be separated from other bacterial actions during infection, a successful approach may involve vaccination against the factors involved in bacterial adhesion such as the components and effectors of the type III secretion machinery.
From page 55...
... A. & Bishop J


This material may be derived from roughly machine-read images, and so is provided only to facilitate research.
More information on Chapter Skim is available.