Prospects for a vaccine against Chlamydia genital disease I. — Microbiology and pathogenesis

Bavoil, Patrik M.; Hsia, Ru-ching; Rank, Roger G.

doi:10.1016/0020-2452(96)85299-7

Cited by 43 publications

(42 citation statements)

References 306 publications

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“…Therefore, chlamydiae appear to use all avenues available for entry, including receptor-mediated endocytosis in clathrin-coated pits, especially in polarized epithelial cells (Wyrick et al, 1989), pinocytosis in non-clathrin-coated pits (Prain and Pearce, 1989) and phagocytosis (Byrne and Moulder, 1978;Ward and Murray, 1984). Several adhesins for mediating receptor-mediated endocytosis and pinocytosis have been proposed, but the data are controversial; the details can be found in excellent recent reviews by Bavoil et al (1996) and Hackstadt (1999). There is no evidence for macropinocytosis of chlamydia, whereby a`triggered' entry (Finlay and Cossart, 1997) induces actin activation, rearrangement and membrane ruffling, as described for Salmonella typhimurium (Francis et al, 1993), or evidence of a major upheaval of host apical membrane, such as microvillus effacement seen with enteropathogenic Escherichia coli (EPEC) (Jerse et al, 1990).…”

Section: Entrymentioning

confidence: 99%

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Intracellular survival by Chlamydia . Microreview

2000

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Section: Entrymentioning

confidence: 99%

“…Important details as well as differences among the species, which account for variations in biological phenomena and, ultimately, probably disease outcome, can be found in excellent reviews (McClarty, 1994;Raulston, 1995;Bavoil et al, 1996;Hatch, 1996;Hackstadt et al, 1997;Sinai and Joiner, 1997;Stephens et al, 1998;Hackstadt, 1999).…”

Section: Introductionmentioning

confidence: 99%

Intracellular survival by Chlamydia . Microreview

2000

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“…Chlamydia species are causative agents of a large spectrum of diseases in humans and animals (7,9,49). There are four known species of Chlamydia: C. trachomatis, C. psittaci, C. pneumoniae, and C. pecorum.…”

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confidence: 99%

Role of Bcl-2 Family Members in Caspase-Independent Apoptosis duringChlamydiaInfection

Perfettini

Reed

Israël³

et al. 2002

Infect Immun

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Infection with an obligate intracellular bacterium, the Chlamydia trachomatis lymphogranuloma venereum (LGV/L2) strain or the guinea pig inclusion conjunctivitis serovar of Chlamydia psittaci, leads to apoptosis of host cells. The apoptosis is not affected by a broad-spectrum caspase inhibitor, and caspase-3 is not activated in infected cells, suggesting that apoptosis mediated by these two strains of Chlamydia is independent of known caspases. Overexpression of the proapoptotic Bcl-2 family member, Bax, was previously shown to induce caspase-independent apoptosis, and we find that Bax is activated and translocates from the cytosol to the mitochondria in C. psittaci-infected cells. C. psittaci-induced apoptosis is inhibited in host cells overexpressing Bax inhibitor-1 and is inhibited through overexpression of Bcl-2, which blocks both caspase-dependent and -independent apoptosis. As Bax and mitochondria are ideally located to sense stress-related metabolic changes emanating from the interior of an infected cell, it is likely that Bax-dependent apoptosis may also be observed in cells infected with other intracellular pathogens.

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“…In humans, the most common consequence of chlamydial genital infection is salpingitis, which can lead to tubal obstruction and infertility (4). In controlled studies in guinea pigs and mice (3,9,38), bacteria are initially detected in the cervical epithelium, but the pathology ascends in most animals to the endometrium and the oviducts within 7 to 9 days after intravaginal inoculation, culminating often in infertility.…”

mentioning

confidence: 99%

Effect ofChlamydia trachomatisInfection and Subsequent Tumor Necrosis Factor Alpha Secretion on Apoptosis in the Murine Genital Tract

Perfettini¹,

Darville

Gachelin³

et al. 2000

Infect Immun

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The pathology observed during Chlamydia infection is due initially to localized tissue damage caused by the infection itself, followed by deleterious host inflammatory responses that lead to permanent scarring. We have recently reported that the infection by Chlamydia in vitro results in apoptosis of epithelial cells and macrophages and that infected monocytes secrete the proinflammatory cytokine interleukin-1␤. At the same time, proinflammatory cytokines such as tumor necrosis factor alpha (TNF-␣) can also trigger apoptosis of susceptible cells. To study the possible relationship between Chlamydia trachomatis infection and apoptosis in vivo, we used the terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling technique to determine whether infection may cause apoptosis in the genital tract of mice and, conversely, whether cytokines produced during the inflammatory response may modulate the level of apoptosis. Our results demonstrate that infected cells in the endocervix at day 2 or 7 after infection are sometimes apoptotic, although there was not a statistically significant change in the number of apoptotic cells in the endocervix. However, large clumps of apoptotic infected cells were observed in the lumen, suggesting that apoptotic cells may be shed from the endocervix. Moreover, there was a large increase in the number of apoptotic cells in the uterine horns and oviducts after 2 or 7 days of infection, which was accompanied by obvious signs of upper tract pathology. Interestingly, depletion of TNF-␣ led to a decrease in the level of apoptosis in the uterine horns and oviducts of animals infected for 7 days, suggesting that the inflammatory cytokines may exert part of their pathological effect via apoptosis in infected tissues.

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Prospects for a vaccine against Chlamydia genital disease I. — Microbiology and pathogenesis

Cited by 43 publications

References 306 publications

Intracellular survival by Chlamydia . Microreview

Intracellular survival by Chlamydia . Microreview

Role of Bcl-2 Family Members in Caspase-Independent Apoptosis duringChlamydiaInfection

Effect ofChlamydia trachomatisInfection and Subsequent Tumor Necrosis Factor Alpha Secretion on Apoptosis in the Murine Genital Tract

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