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Chapter 13 : In Vivo Chlamydial Infection

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Abstract:

This chapter briefly summarizes animal models and biomathematical models and addresses their potential uses. Although there is a wide spectrum of diseases caused by , the majority of animal model research has centered on models of genital infection; therefore, the focus of the chapter is on models of genital infections, but other models are discussed where relevant. The major application of animal models of chlamydial infection has been directed toward the characterization of the host response and the understanding of the mechanisms of protective immunity, all oriented toward the development of an effective vaccine. Perhaps the most intriguing biological characteristic of chlamydiae is their biphasic developmental cycle. Beginning with the morphologic appearance of the various stages of the cycle, there has been an immense amount of ultrastructural work performed in vitro to characterize the structure of reticulate bodies (RBs) and elementary bodies (EBs). Low-magnification pictures showed a strong acute inflammatory response with polymorphonuclear leukocytes (PMNs) often in the vicinity of infected cells. With the capabilities today to accumulate massive amounts of qualitative and quantitative data from many different components of host and pathogen physiology, it should be possible to construct biomathematical models that can then be used to evaluate hypotheses in silico.

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13

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Figures

Image of FIGURE 1
FIGURE 1

Events occurring 24 hours and 30 hours after infection. (A) At 24 hours, multiple early inclusions containing one to a few RBs are seen. Some epithelial cells contain multiple inclusions. RBs are clearly dividing, and the proximity of inclusions suggests that the fusion process is under way (arrows). (B) Inclusion with multiple RBs at 30 hours after infection and PMNs (P) in contact with the infected epithelial host cell. Scale bars for both panels, 2 µm. doi:10.1128/9781555817329.ch13.f1

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13
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Image of FIGURE 2
FIGURE 2

Events at 36 hours after infection. (A) Multiple large mature inclusions are seen. In particular, one infected cell (arrow) is being detached from the epithelium with a PMN (P) directly in the space beneath the cell, giving the appearance of “pushing” the cell off of the epithelial surface; the PMN appears to have phagocytized numerous RBs. Nuclei (N) of the infected cells are visible. (B) Terminal infected cell with chlamydiae distributed in the cytosol. The cell appears to be in the process of being dislodged from the epithelial layer. Scale bars: panel A, 10 µm; panel B, 2 µm. doi:10.1128/9781555817329.ch13.f2

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13
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Image of FIGURE 3
FIGURE 3

PMNs enter into the infected host epithelial cell to make direct contact with chlamydiae. At 42 hours after infection, the inclusion membrane is no longer visible and the intracellular PMN is in direct contact with chlamydiae. Note the projections from the PMNs touching the IBs or EBs (arrows). Scale bar: 2 µm. doi:10.1128/9781555817329.ch13.f3

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13
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Image of FIGURE 4
FIGURE 4

Schematic in vivo development of . At 18 h, host cells containing internalized EBs are shown, with some in the process of becoming RBs. At 24 h, multiple small inclusions are present. At 30 h, fusion of inclusions has occurred and inclusions contain primarily RBs. At 36 h, inclusions have increased in size with ongoing differentiation of RBs into EBs. At 42 to 48 h, termination of the developmental cycle occurs by three specific mechanisms. (A) The inclusion membrane disintegrates, leaving organisms free in the cytosol. The cell is dislodged from the epithelial layer and breaks apart, allowing EBs to attach to uninfected cells. (B) PMNs attracted to the site effect detachment of the infected cell from the epithelial layer likely through the action of matrix-metalloprotease 9. In some cases, the host cell and inclusion are intact so that the entire cell becomes free in the lumen. Ultimately, the cell dies, releasing EBs at the same or a distant site. (C) The PMN may actually enter the host cell in “pursuit” of chlamydiae. The host cell will die as a result of the enzymes released by the PMN with release of EBs into the lumen. doi:10.1128/9781555817329.ch13.f4

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13
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Image of FIGURE 5
FIGURE 5

Inclusion at 42 hours after infection. Note that the majority of the RBs in this inclusion (arrow) are along the periphery of the inclusion adjacent to the inclusion membrane while the EBs are in the internal area. Scale bar: 10 µm. doi:10.1128/9781555817329.ch13.f5

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13
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Image of FIGURE 6
FIGURE 6

Stressed inclusions were observed in the cervix of a mouse depleted of PMNs by antibody treatment. Note the large aberrant RBs (AB) as well as packets of miniature RBs (black arrow). Also, the stressed inclusion is devoid of granular material representing glycogen accumulation. Lipid bodies (L) can be observed associated with the inclusion and apparently entering the inclusion. Scale bar: 2 µm. doi:10.1128/9781555817329.ch13.f6

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13
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References

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Tables

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TABLE 1

Major animal models

Citation: Rank R. 2012. In Vivo Chlamydial Infection, p 285-310. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch13

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