Heparin‐binding outer membrane protein of chlamydiae

Stephens, Richard S.; Koshiyama, Kelli; Lewis, Elizabeth; Kubo, Aya

doi:10.1046/j.1365-2958.2001.02418.x

Cited by 63 publications

(67 citation statements)

References 42 publications

(66 reference statements)

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“…Furthermore, FGF2 enhances binding of Chlamydia in an heparan sulfate proteoglycan-dependent manner (37). Candidate Chlamydia proteins involved in these interactions include the Chlamydia OmcB protein, which binds to glycosaminoglycans, such as heparan sulfate (38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

Attachment ofChlamydia trachomatisL2 to host cells requires sulfation

Rosmarin

Carette

Olive

et al. 2012

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

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Chlamydia trachomatis is a pathogen responsible for a prevalent sexually transmitted disease. It is also the most common cause of infectious blindness in the developing world. We performed a loss-of-function genetic screen in human haploid cells to identify host factors important in C. trachomatis L2 infection. We identified and confirmed B3GAT3 , B4GALT7 , and SLC35B2 , which encode glucuronosyltransferase I, galactosyltransferase I, and the 3′-phosphoadenosine 5′-phosphosulfate transporter 1, respectively, as important in facilitating Chlamydia infection. Knockout of any of these three genes inhibits Chlamydia attachment. In complementation studies, we found that the introduction of functional copies of these three genes into the null clones restored full susceptibility to Chlamydia infection. The degree of attachment of Chlamydia strongly correlates with the level of sulfation of the host cell, not simply with the amount of heparan sulfate. Thus, other, as-yet unidentified sulfated macromolecules must contribute to infection. These results demonstrate the utility of screens in haploid cells to study interactions of human cells with bacteria. Furthermore, the human null clones generated can be used to investigate the role of heparan sulfate and sulfation in other settings not limited to infectious disease.

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Section: Discussionmentioning

confidence: 99%

Attachment ofChlamydia trachomatisL2 to host cells requires sulfation

Rosmarin

Carette

Olive

et al. 2012

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

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“…Considerable evidence suggests that electrostatic interactions are involved in an initial, reversible interaction with the eukaryotic host cell for many, but not all strains and species of chlamydiae [26,28,30]. Initial reversible attachment to heparan sulfate-like glycosaminoglycans is followed by irreversible binding to an unknown secondary receptor and this leads to the recruitment of actin to the attachment site, formation of an actin-rich, pedestallike structure, and finally internalization of the bacteria [10].…”

Section: Discussionmentioning

confidence: 99%

Effect of ovotransferrin and lactoferrins onChlamydophila psittaciadhesion and invasion in HD11 chicken macrophages

et al. 2007

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-The effect of ovotransferrin (ovoTF), human lactoferrin (hLF) and bovine lactoferrin (bLF) on the obligate intracellular pathogen Chlamydophila (Cp.) psittaci was evaluated using a model of Buffalo Green Monkey kidney (BGM) cells and HD11 chicken macrophages as artificial hosts. Firstly, the effect of transferrins on the infectivity of the bacteria was evaluated. Pre-incubation of Cp. psittaci with 0.5 to 5 mg/mL ovoTF prior to infecting BGM cells significantly lowered the infection rate (P < 0.05). For both lactoferrins, the infection rate could only be reduced with 5 mg/mL, albeit not significantly as compared to the infection rate created by the untreated bacteria. Secondly, transferrins were tested for their ability to influence bacterial adhesion and entry in HD11 cells. Maximal non-cytotoxic and non-bactericidal concentrations of 0.05 mg/mL ovoTF and 0.5 mg/mL hLF and bLF were used. Overall, ovoTF was more effective than human and bovine LF in inhibiting bacterial irreversible attachment and cell entry and the latter was accompanied by a dose-dependent reduction of actin recruitment at the bacterial entry site. However, once bacteria had entered HD11 cells, transferrins had apparently no effect on intracellular replication. The present findings suggest a possible role for transferrins and especially ovoTF, in preventing avian Cp. psittaci infections.ovotransferrin / lactoferrin / Chlamydia / Chlamydophila psittaci

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“…The developmental cycle consists of infectious and noninfectious stages that exhibit unique morphological, biochemical, and biological properties. The infectious elementary body (EB) is a metabolically inactive particle with a rigid, disulfide cross-linked outer membrane (OM) (9)(10)(11)(12) that enables the EB to attach to and enter host cells (13)(14)(15). After host cell entry, the EB is localized to a phagosome, and the primary differentiation process is initiated.…”

mentioning

confidence: 99%

Genomic transcriptional profiling of the developmental cycle of Chlamydia trachomatis

Belland

Zhong

Crane

et al. 2003

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

449

544

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Chlamydia trachomatis is one of the most common bacterial pathogens and is the etiological agent of debilitating sexually transmitted and ocular diseases in humans. The organism is an obligate intracellular prokaryote characterized by a highly specialized biphasic developmental cycle. We have performed genomic transcriptional analysis of the chlamydial developmental cycle. This approach has led to the identification of a small subset of genes that control the primary (immediate-early genes) and secondary (late genes) differentiation stages of the cycle. Immediate-early gene products initiate bacterial metabolism and potentially modify the bacterial phagosome to escape fusion with lysosomes. One immediate early gene (CT147) is a homolog of the human early endosomal antigen-1 that is localized to the chlamydial phagosome; suggesting a functional role for CT147 in establishing the parasitophorous vacuole in a nonfusogenic pathway. Late gene products terminate bacterial cell division and constitute structural components and remodeling activities involved in the formation of the highly disulfide cross-linked outer-membrane complex that functions in attachment and invasion of new host cells. Many of the genes expressed during the immediate-early and late differentiation stages are Chlamydia-specific and have evolutionary origins in eukaryotic lineages.T he Chlamydia trachomatis bacterium is an obligate intracellular pathogen of humans that primarily infects columnar epithelial cells of the ocular and genital mucosae. Chlamydial infections of the eye and genital tract have a significant impact on human health worldwide, causing trachoma, the leading cause of preventable blindness, and sexually transmitted diseases (STD) that include pelvic inflammatory disease and tubal factor infertility (1, 2). Chlamydial STDs are also risk factors in cervical squamous cell carcinoma (3) and HIV infection (4, 5).C. trachomatis has a small genome of Ϸ1 Mb encoding 893 chromosomal and 8 plasmid ORFs that share significant homology in both gene structure and order among strains that infect human and animal hosts (6, 7). Two distinguishing characteristics of this pathogen are its developmental cycle and predilection for causing persistent infections (8). The developmental cycle consists of infectious and noninfectious stages that exhibit unique morphological, biochemical, and biological properties. The infectious elementary body (EB) is a metabolically inactive particle with a rigid, disulfide cross-linked outer membrane (OM) (9-12) that enables the EB to attach to and enter host cells (13-15). After host cell entry, the EB is localized to a phagosome, and the primary differentiation process is initiated. This developmental process involves the commencement of bacterial metabolism and the conversion of the EB to the intracellular replicating form of the organism, termed the reticulate body (RB).At the very early stage of infection (1-3 h) the parasite exerts profound effects on the host. Through an unknown mechanism, dependent on both ba...

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Heparin‐binding outer membrane protein of chlamydiae

Cited by 63 publications

References 42 publications

Attachment ofChlamydia trachomatisL2 to host cells requires sulfation

Attachment ofChlamydia trachomatisL2 to host cells requires sulfation

Effect of ovotransferrin and lactoferrins onChlamydophila psittaciadhesion and invasion in HD11 chicken macrophages

Genomic transcriptional profiling of the developmental cycle of Chlamydia trachomatis

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