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Chapter 16 : Cell Biology of Salmonella Pathogenesis

Author: B. Brett Finlay1
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Affiliations: 1: Biotechnology Laboratory and Departments of Biochemistry and Microbiology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3
Content Type: Monograph
Publication Year: 1994

Category: Microbial Genetics and Molecular Biology; Bacterial Pathogenesis

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Abstract:

species are masters at subverting various host processes for their own use. The interactions that occur between species and host cells are complex. They have been studied more extensively with nonphagocytic cells such as epithelial cells than with macrophages, although some of the processes are common between these two cell types. For the review in this chapter, the author has concentrated on the events that occur in the host cell rather than to focus on the bacterial genes that mediate these events. Study of the cell biology of these interactions has revealed several interesting processes and provided new tools for the study of eukaryotic cell function. It has recently been shown that species trigger extensive membrane ruffling and macropinocytosis in macrophages and enter into a spacious phagosome. Bacterial invasins appear to significantly enhance uptake into phagocytic cells such as macrophages, since noninvasive mutants have decreased levels of invasion into cultured macrophages. One recurring theme about all of these exploitations of host cell function is that the bacteria achieve the desired effect by "nonconventional" mechanisms, as viewed by cell biologists. The advancement of this field is heavily dependent on other fields, especially cell biology. In addition, further characterization of the bacterial products that are involved in the various stages of infection will enhance the cell biology studies.

Citation: Finlay B. 1994. Cell Biology of Salmonella Pathogenesis, p 249-261. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch16
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Cell Biology of Salmonella Pathogenesis
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Citation: Finlay B. 1994. Cell Biology of Salmonella Pathogenesis, p 249-261. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch16
/content/10.1128/9781555818340.chap16.fig16-1
Figure 1

Transmission electron micrograph of entering polarized Caco-2 human intestinal epithelial cells. Note the microvillus distortions and the bacterium localized within membrane-bound inclusions. Bar, 1 μm.

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10.1128/9781555818340/fig16-1.gif
Image of Figure 1
Figure 1

Transmission electron micrograph of entering polarized Caco-2 human intestinal epithelial cells. Note the microvillus distortions and the bacterium localized within membrane-bound inclusions. Bar, 1 μm.

Citation: Finlay B. 1994. Cell Biology of Salmonella Pathogenesis, p 249-261. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch16
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Figure 2

triggers capping of host membrane proteins in HeLa cells. (A) Phase-contrast micrograph of invading HeLa cells after 30 min. (В) Corresponding fluorescent micrograph after staining with antibodies to the cell surface-associated marker, the class I major histocompatibility complex. Note the capped localization of this marker corresponding to the area of bacterial invasion. Bar, 10 μm.

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10.1128/9781555818340/fig16-2.gif
Image of Figure 2
Figure 2

triggers capping of host membrane proteins in HeLa cells. (A) Phase-contrast micrograph of invading HeLa cells after 30 min. (В) Corresponding fluorescent micrograph after staining with antibodies to the cell surface-associated marker, the class I major histocompatibility complex. Note the capped localization of this marker corresponding to the area of bacterial invasion. Bar, 10 μm.

Citation: Finlay B. 1994. Cell Biology of Salmonella Pathogenesis, p 249-261. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch16
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Figure 3

Fluorescent confocal micrograph of filamentous structures in HeLa epithelial cells infected with . Cells were infected for 6 h and then fixed and labeled with antibodies to a lysosomal glycoprotein (Igp) (A) or anti- lipopolysaccharide (B). Note the blebs associated with the filamentous structures distal to intracellular bacteria. Bar, 10 μm.

10.1128/9781555818340/fig16-3_thmb.gif
10.1128/9781555818340/fig16-3.gif
Image of Figure 3
Figure 3

Fluorescent confocal micrograph of filamentous structures in HeLa epithelial cells infected with . Cells were infected for 6 h and then fixed and labeled with antibodies to a lysosomal glycoprotein (Igp) (A) or anti- lipopolysaccharide (B). Note the blebs associated with the filamentous structures distal to intracellular bacteria. Bar, 10 μm.

Citation: Finlay B. 1994. Cell Biology of Salmonella Pathogenesis, p 249-261. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch16
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