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Color Plates

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Figures

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Color Plate 1

(chapter 7) A section of small intestinefrom a patient with Whipple's disease examined withconfocal fluorescence microscopy at 3,000× magnification.Intestinal epithelial cells are located in the upperright corner of these images, with the mucosa in thelower left. Yo-Pro nucleic acid stain (green) highlightshost cell nuclei and bacterial nucleic acids, revealingmultiple small bacillary bodies free in the lamina propria.A -specific rDNA probe labeled with Cy-5and targeting bacterial rRNA (blue) reveals clumps ofbacteria in the lamina propria. Most bacteria appear justbasal to the intestinal epithelial cells, forming a continuousband.

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 2

(chapter 7) A sectionof small intestine from a patient withWhipple's disease subjected to fluorescencein situ hybridization and visualizedat 400× magnification usinga confocal microscope. Nucleic acidsare stained green with Yo-Pro dye, rRNA appears blue usinga Cy-5-labeled rDNA probe, and thehuman intracellular cytoskeletal proteinvimentin appears red using aTexas red-labeled antivimentin antibody.Only cells of mesenchymal originhave vimentin; hence, epithelialcells do not stain with the antivimentinantibody, but macrophages in thelamina propria do contain vimentin.Most of the rRNA signal from bacteriaappears in the extracellular compartment.

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 3

(chapter 13) Activation of pathogenic mucosal immune responses leading tochronic intestinal inflammation in genetically susceptible hosts. Acquired or intrinsic enhancedmucosal permeability enhances uptake of luminal bacterial adjuvants and antigens, which activatelamina propria innate and cognate immune cells. Resultant proinflammatory cytokinescause tissue injury, which initiates a self-perpetuating inflammatory response driven by an everincreasinguptake of microbial antigens. Genetic susceptibility is mediated by defective immunoregulationor barrier function. Used with permission from the AGA.

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 4

(chapter 13) Activation of NF-B by bacterial components binding to patternrecognition receptors. Bacterial cell wall polymers selectively bind to membrane TLR orintracytoplasmic NOD-1 and NOD-2 to initiate signaling of a cascade of kinases resulting inactivation of NF-B. PG-PS bind to TLR-2 while LPS binds to TLR-4; both LPS and PGPSbind to NOD-1 and NOD-2. Signal transduction activates NF-B to induce transcriptionof a number of proinflammatory gene products. Used with permission from the AGA.

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 5

(chapter 13) Induction of self-limited versus chronic intestinal inflammationin normal versus genetically susceptible hosts, respectively, following a transient injury. Nonspecificinjury due to an acute infection or exposure to nonsteroidal anti-inflammatory drugs(NSAID) leads to acute inflammation in all hosts. Genetically resistant (normal) hosts rapidlyheal mucosal injury with no residual damage. In contrast, genetically susceptible hosts withdysregulated immune responses or defective mucosal barrier function/healing develop chronicinflammation due to constant antigenic stimulation of aggressive immune responses. Used withpermission from the AGA.

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 6

(chapter 17) Effect of the SPATE toxin Pet on the epithelial cytoskeleton.Hep-2 cells were incubated with 30 nM purified Pet toxin on ice, then shifted to 37°C for2 h. Cells were then fixed and stained with rhodamine-phalloidin and with mouse anti-spectrinmonoclonals, followed by fluorescein isothiocyanate (FITC)-conjugated anti-mouse immunoglobulin.Cells were visualized under confocal microscopy. Actin stress fibers appear redand spectrin green. (A) Merge of images for unintoxicated Hep-2 cells. Spectrin localizes tothe membrane cytoskeleton and therefore stains diffusely. (B through D) Pet-intoxicated cell.(B) When visualized for actin, stress fibers are still apparent, although the cell has begun tomanifest actin-containing lamellipodium-like structures. (C) Spectrin appears condensed andperipherally localized, with formation of spectrin-containing blebs. (D) Merge of images Band C. Actin filaments are seen condensed in areas of bleb formation. (R. Cappello and J.Nataro, unpublished observations.)

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 7

(chapter 19) Immunohistochemical localization of Gal1 receptors andthe p65 subunit of NF-B on mouse colonic epithelium in EHEC-infected mice.Colonic epithelium of noninfected mice (a and d) shows no evidence of either Gal1receptor or NF-B p65 subunit immunoreactivity. However, 3 days after infectionwith EHEC, increased expression of both Gal1 receptors and NF-B is evident (b ande). Administration of the NF-B inhibitor dexamethasone during EHEC infectiondiminishes expression of Gal1 receptor and NF-_B activation in colonic epithelial cells,indicating that Gal1 receptor upregulation in response to EHEC is mediating via NF-B. Magnification, ×400. (From reference 39, with permission.)

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 8

(chapter 28) Rotavirus genes, proteins, and viral structure. (a) Pattern ofseparation of the 11 segments of rotavirus RNA after electrophoresis on a polyacrylamide gel,giving the names of the proteins encoded in each segment. Proteins found in virus particles(VP1 through 7) and nonstructural proteins (NSP1 through NSP6) found only in infectedcells are shown. (b) Surface representation of the rotavirus structure. Three types of channels(I, II, III), the VP4 spikes, and the VP7 capsid layer are highlighted by arrows. (c) Cutawaystructure illustrating the internal VP6 and VP2 layers. The flower-shaped VP1/VP3 complex,attached to the inside of the VP2 layer, is also shown. (d) Structural organization of thegenomic double-stranded RNA. The outer layer of RNA has a dodecahedral appearance. (e)Structure of double-layered particles transcribing mRNAs that exit the virus through the typeI channels at the fivefold vertices. (f ) Cutaway view depicting the exit pathway of mRNA inone of the channels. Viral structures provided by B. V. V. Prasad.

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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Color Plate 9

(chapter 28) Norwalk virus structure. VLPs (top left) visualized by negativestainelectron microscopy have a surface structure that consists of 90 dimeric arches that emanatefrom the surface of the particles (top right). A ribbon diagram of a monomer of thecapsid protein (lower right) shows it is composed of a shell domain connected to a protrudingdomain that has two subdomains. The N terminus is inside particles, while the C terminus isexposed in the hollows made by dimers of the capsid protein (lower left). Viral structureskindly provided by B. V. V. Prasad.

Citation: Hecht G. 2003. Color Plates, In Microbial Pathogenesis and the Intestinal Epithelial Cell. ASM Press, Washington, DC.
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