The chlamydial developmental cycle: Figure 1

AbdelRahman, Yasser M.; Belland, Robert J.

doi:10.1016/j.femsre.2005.03.002

Cited by 541 publications

(489 citation statements)

References 96 publications

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“…pneumoniae is an obligate intracellular pathogen, which can exist as a persistent asymptomatic infection, resulting in chronic inflammation [92]. As described above, inflammation is a key facet of AMD pathogenesis and thus, with regard to studies demonstrating the presence of C. pneumoniae in retina of AMD CNV, the question arises whether these C. pneumoniae play a role in pathogenesis or whether they are coincidentally carried to the lesions by macrophages responding to or mediating other pathologic events.…”

Section: Chlamydia Pneumoniae Infection and Amdmentioning

confidence: 99%

Immunopathological aspects of age-related macular degeneration

2008

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Age-related macular degeneration (AMD) represents a leading cause of blindness worldwide. While the clinical and histopathological aspects of AMD are well characterized, its etiology and pathogenesis remain unclear. Recent findings suggest a role for immunologic processes in AMD pathogenesis, including the age-related generation of extracellular deposits inside the Brusch membrane and beneath the retinal pigment epithelium, recruitment of macrophages for clearance of these deposits, complement activation, recruitment of tissue-destructive macrophages, microglial activation and accumulation, and proinflammatory effects of chronic inflammation by Chlamydia pneumoniae. This review discusses the evidence for the role of inflammation in human AMD and in animal models of AMD.

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Section: Chlamydia Pneumoniae Infection and Amdmentioning

confidence: 99%

Immunopathological aspects of age-related macular degeneration

2008

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“…The RBs replicate by binary fission and then, 18Ϫ48 h postinfection (p.i. ), depending on the species, start to redifferentiate back to EBs and exit the cell to repeat the cycle (5).…”

mentioning

confidence: 99%

Transformation and isolation of allelic exchange mutants of Chlamydia psittaci using recombinant DNA introduced by electroporation

Binet

Maurelli

2009

Proc. Natl. Acad. Sci. U.S.A.

106

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To facilitate genetic investigations in the obligate intracellular pathogens Chlamydia, the ability to construct variants by homologous recombination was investigated in C. psittaci 6BC. The single rRNA operon was targeted with a synthetic 16S rRNA allele, harboring three nucleotide substitutions over 398 bp, which imparts resistance to kasugamycin (Ksm) and spectinomycin (Spc) and causes loss of one HpaI restriction site. A fourth, silent mutation was introduced 654 bp downstream in the beginning of the 23S rRNA gene. C. psittaci 6BC infectious particles were electroporated with various concentrations of circular or linearized plasmids containing different lengths of the rRNA region homologous to the chromosomal copy except for the four nucleotide substitutions. Ksm and Spc were added 18 h after inoculation onto confluent cell monolayers in the plaque assay. Resistant plaques were picked and expanded with selection 10 days later before collecting DNA for analysis by PCR, restriction mapping, sequencing, or Southern. Spontaneous resistance to Ksm and Spc was never observed in mock electroporated bacteria (frequency <6.2 ؋ 10 ؊9 ). Conversely, double resistance and replacement of the 16S rRNA gene were observed when C. psittaci was electroporated with the recombination substrates. Highest efficiency was obtained with 10 g of circular vector prepared in a DNA methylase-deficient Escherichia coli (1.9 ؎ 1.1 ؋ 10 ؊6 , n ‫؍‬ 7). Coinheritance of the silent 23S rRNA mutation was seen in 46 of 67 recombinants analyzed, illustrating DNA exchange of up to 1,052 bp in length. These findings provide the first step toward genetic manipulation of Chlamydia.recombination ͉ selection ͉ plaque assay

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“…Chlamydia infections begin with the attachment of an elementary body (EB), the invasive but non-replicative form of the pathogen, to epithelial cells of the genital tract. Shortly after entry, EBs transition into metabolically active reticulate bodies (RBs) that replicate within a membrane-bound bound pathogenic vacuole termed an "inclusion" (8). Midway through the infectious cycle, replication becomes asynchronous, with some RBs transitioning back to the infectious EB stage (8).…”

mentioning

confidence: 99%

“…Shortly after entry, EBs transition into metabolically active reticulate bodies (RBs) that replicate within a membrane-bound bound pathogenic vacuole termed an "inclusion" (8). Midway through the infectious cycle, replication becomes asynchronous, with some RBs transitioning back to the infectious EB stage (8). Eventually, EBs are released into the extracellular space to initiate subsequent rounds of infection in adjacent cells.…”

mentioning

confidence: 99%

cPLA2 Regulates the Expression of Type I Interferons and Intracellular Immunity to Chlamydia trachomatis

Vignola

Kashatus

Taylor

et al. 2010

Journal of Biological Chemistry

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Infection with the obligate bacterial intracellular pathogenChlamydia trachomatis leads to the sustained activation of the small GTPase RAS and many of its downstream signaling components. In particular, the mitogen-activated protein kinase ERK and the calcium-dependent phospholipase cPLA 2 are activated and are important for the onset of inflammatory responses. In this study we tested if activation of ERK and cPLA 2 occurred as a result of RAS signaling during infection and determined the relative contribution of these signaling components to chlamydial replication and survival. We provide genetic and pharmacological evidence that during infection RAS, ERK, and, to a lesser extent, cPLA 2 activation are uncoupled, suggesting that Chlamydia activates individual components of this signaling pathway in a non-canonical manner. In human cell lines, inhibition of ERK or cPLA 2 signaling did not adversely impact C. trachomatis replication. In contrast, in murine cells, inhibition of ERK and cPLA 2 played a significant protective role against C. trachomatis. We determined that cPLA 2 -deficient murine cells are permissive for C. trachomatis replication because of their impaired expression of ␤ interferon and the induction of immunity-related GTPases (IRG) important for the containment of intracellular pathogens. Furthermore, the MAPK p38 was primarily responsible for cPLA 2 activation in Chlamydia-infected cells and IRG expression. Overall, these findings define a previously unrecognized role for cPLA 2 in the induction of cell autonomous cellular immunity to Chlamydia and highlight the many non-canonical signaling pathways engaged during infection.

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The chlamydial developmental cycle: Figure 1

Cited by 541 publications

References 96 publications

Immunopathological aspects of age-related macular degeneration

Immunopathological aspects of age-related macular degeneration

Transformation and isolation of allelic exchange mutants of Chlamydia psittaci using recombinant DNA introduced by electroporation

cPLA2 Regulates the Expression of Type I Interferons and Intracellular Immunity to Chlamydia trachomatis

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