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Chapter 18 : Cellular Biology of Infection

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Abstract:

In this chapter, the molecular and cellular biology of infection is reviewed and, at the end, a model which attempts to bridge the immunology with the pathogenesis is discussed. A number of factors facilitate in vitro assays. First, and most importantly, actually grows intracellularly. Second, gentamicin can be used to sterilize the extracellular medium without affecting the intracellular growth rate. Third, the infection of host cells is relatively nontoxic, so that cells do not detach from the substrate and gentamicin does not enter the cell cytoplasm. Lastly, the stages in the infection can be examined and quantitated by electron microscopy and video microscopy. The current model also has serious implications for the nature of antigen presentation. Current models describe two distinct pathways of antigen presentation. The first involves the processing of antigens within an acidic vacuolar compartment and presentation to CD4 T cells in the context of major histocompatibility complex (MHC) class II antigens. The second involves presentation of cytosolic antigens and presentation to CD8 T cells in the context of MHC class I antigens. Nevertheless, all mutants which enter the cytoplasm were shown to immunize mice to subsequent challenge. Thus, the data are consistent with the requirement that the organism must enter the cytoplasm for the induction of immunity. Whether entry into the cytoplasm is sufficient for long-lived immunity or whether cell-to-cell spread is also necessary remains to be determined.

Citation: Portnoy D. 1994. Cellular Biology of Infection, p 279-293. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch18

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Major Histocompatibility Complex
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Immune Systems
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Figure 1

Model for the intracellular life cycle of The stippled material represents polymerized actin. Adapted from Tilney and Portnoy ( ), with copyright permission of the Rockefeller University Press.

Citation: Portnoy D. 1994. Cellular Biology of Infection, p 279-293. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch18
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Image of Figure 2
Figure 2

regulon of Genes are represented by large arrows, transcripts are represented by wavy lines, putative PrfA-binding sites are represented by small boxes containing short arrows, and putative rho-independent terminators are represented by a short post terminated by a circle. PrfA protein is shown as a dimer, although this has not been demonstrated. This model is based on information presented in previous publications ( ).

Citation: Portnoy D. 1994. Cellular Biology of Infection, p 279-293. In Miller V, Kaper J, Portnoy D, Isberg R (ed), Molecular Genetics of Bacterial Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555818340.ch18
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