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Chapter 5 : Cell Biology

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Abstract:

Chlamydiae are extremely successful pathogens of humans and animals. The chlamydial developmental cycle may be considered superficially analogous to bacterial sporulation in that it consists of an environmentally stable cell type, called the elementary body (EB), and a functionally and morphologically distinct vegetative cell type, termed the reticulate body (RB). Electrostatic interactions play an important role in at least the initial stages of infection. Attachment is dependent upon cations to neutralize the net negative surface charge of both host and parasite. Several chlamydial components have been proposed at one time or another to function as adhesins. A number of EB surface components have been proposed as potential ligands mediating attachment to host cells. Currently, heparan sulfate-like proteoglycans are considered one of the more promising candidates mediating at least an initial electrostatic interaction between the EB and the host cell surface. The general implication is that chlamydiae, like many other intracellular pathogens, similarly stimulate signal transduction pathways, including tyrosine phosphorylation of host proteins involved in rearrangements of the actin skeleton to promote entry. This chapter talks about intracellular development. Intracellular parasites have evolved diverse strategies for evasion of host cellular defense mechanisms associated with adaptations for survival in distinct intracellular compartments. The chapter discusses effects of the host cell. It is essential that chlamydiae maintain the integrity of the host cell for the duration of their intracellular growth because they are obligate intracellular parasites.

Citation: Hackstadt T. 1999. Cell Biology, p 101-138. In Stephens R (ed), Chlamydia. ASM Press, Washington, DC. doi: 10.1128/9781555818203.ch5
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Figure 1

The developmental cycle. Infection is initiated by EBs. Immediately after endocytosis, EBs are found within tightly associated membrane vesicles (0 Hr). Within a few hours, EBs differentiate into the larger, metabolically active RBs (2 Hr). As the chlamydiae multiply, the inclusion increases in size to accommodate the multiplying bacteria. RBs are typically observed juxtaposed to the inclusion membrane (18 Hr). As the infection progresses, increasing numbers of chlamydiae are observed unattached in the interior of the inclusion (36 Hr). These unattached organisms are, for the most part, EBs and intermediate developmental forms. EBs accumulate within the inclusion even as RBs, still associated with the inclusion membrane, continue to multiply until the cell lyses at 40 to 48 h postinfection. Reprinted from with permission.

Citation: Hackstadt T. 1999. Cell Biology, p 101-138. In Stephens R (ed), Chlamydia. ASM Press, Washington, DC. doi: 10.1128/9781555818203.ch5
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Figure 2

Models of the vesicular interactions of the chlamydial inclusion before (early inclusion) (A) and after (mature inclusion) (B) modification of the host's response as a result of chlamydial polypeptide synthesis. Endocytosed EBs are internalized into a vesicle that displays minimal interaction with the endocytic pathway and is very restricted in its fusion with lysosomes. No interaction with vesicles delivering sphingomyelin or ceramide is initiated. EBs prevented from modifying the vesicle by inhibitors of chlamydial transcription or translation remain within this vesicle and are eventually degraded within lysosomes. By 2 h postinfection, in a process that requires early protein synthesis, actively transforms the properties of the nascent inclusion. Once these modifications have occurred, the inclusion is believed to exhibit the properties of a mature inclusion. Plasma membrane markers, fluid-phase markers, markers for early (transferrin and transferring receptor) and late (cation-independent mannose-6-phosphate receptor) endosomes, or lysosomes (acid phosphatase, cathepsin D, lysosomal glycoproteins, or the vacuolar H-ATPase) are not associated with the chlamydial inclusion. Instead, the chlamydial inclusion fuses with a subset of sphingomyelin-containing vesicles in transit to the plasma membrane. Fusion of these vesicles exposes the sphingomyelin on the luminal surface of the inclusion membrane from which it is adsorbed by the chlamydiae and incorporated into their cell walls.

Citation: Hackstadt T. 1999. Cell Biology, p 101-138. In Stephens R (ed), Chlamydia. ASM Press, Washington, DC. doi: 10.1128/9781555818203.ch5
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