Cell Surface Heparan Sulfate Promotes Replication of
            <i>Toxoplasma gondii</i>

Bishop, Joseph R.; Crawford, Brett E.; Esko, Jeffrey D.

doi:10.1128/iai.73.9.5395-5401.2005

Cited by 24 publications

(13 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This idea is further supported by the finding that treatment of HCT-8 cells with heparinase II, ␤-xyloside, or sodium chlorate reduced C. parvum infection more than attachment alone. Proteoglycans have been implicated in the mediation of intracellular development of T. gondii as well (41). Similar to CpClec-Fc, C. parvum attachment to CHO pgsA-745 and pgsD-677 was comparably reduced, a finding also reported for T. gondii (21), suggesting that intestinal apicomplexan parasites display a higher affinity for HSPGs during infection.…”

Section: Discussionsupporting

confidence: 60%

The Cryptosporidium parvum C-Type Lectin CpClec Mediates Infection of Intestinal Epithelial Cells via Interactions with Sulfated Proteoglycans

Ludington

Ward

2016

Infect Immun

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 60%

The Cryptosporidium parvum C-Type Lectin CpClec Mediates Infection of Intestinal Epithelial Cells via Interactions with Sulfated Proteoglycans

Ludington

Ward

2016

Infect Immun

View full text Add to dashboard Cite

“…In the glucuronosyltransferase-deficient CHO cell line, Toxoplasma replication is retarded (42). In the clones that we obtained, we observed no deficiency in the ability of Chlamydia to replicate in the null clones once access was gained, notwithstanding the deficit in attachment.…”

Section: Discussionmentioning

confidence: 55%

Attachment ofChlamydia trachomatisL2 to host cells requires sulfation

Rosmarin

Carette

Olive

et al. 2012

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

View full text Add to dashboard Cite

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.

show abstract

“…The initial binding to a negatively charged component of the membrane is mediated by the net positive charge of each GRA2 amphipathic α-helix. Although the binding of GRA proteins to the heparan sulfate structure has never been investigated, it was reported that heparan sulfate facilitates the replication of T. gondii in the parasitophorous vacuole (Bishop et al 2005). However, it is logical that the most important binding event occurs during the initial contact between the tachyzoite and the host cell and is, in part, mediated by the tachyzoite SAG family of surface protein and host cell proteoglycans.…”

Section: Discussionmentioning

confidence: 98%

Toxoplasma gondii secretory proteins bind to sulfated heparin structures

Azzouz¹,

Kamena²,

Laurino³

et al. 2012

Glycobiology

View full text Add to dashboard Cite

Toxoplasma gondii is the causative agent of toxoplasmosis, one of the most widespread infections in humans and animals, and is a major opportunistic pathogen in immunocompromised patients. Toxoplasma gondii is unique as it can invade virtually any nucleated cell, although the mechanisms are not completely understood. Parasite attachment to the host cell is a prerequisite for reorientation and penetration and likely requires the recognition of molecules at the host cell surface. It has been reported that the affinity of tachyzoites, the invasive form of T. gondii, for host cells can be inhibited by a variety of soluble-sulfated glycosaminoglycans (GAGs), such as heparan sulfate. Using heparin-functionalized zeolites in the absence of host cells, we visualized heparin-binding sites on the surface of tachyzoites by confocal and atomic force microscopy. Furthermore, we report that protein components of the parasite rhoptry, dense granule and surface bind GAGs. In particular, the proteins ROP2 and ROP4 from the rhoptry, GRA2 from the dense granules and the surface protein SAG1 were found to bind heparin. The binding specificities and affinities of individual parasite proteins for natural heparin and heparin oligosaccharides were determined by a combination of heparin oligosaccharide microarrays and surface plasmon resonance. Our results suggest that interactions between sulfated GAGs and parasite surface antigens contribute to T. gondii attachment to host cell surfaces as well as initiating the invasion process, while rhoptries and dense granule organelles may play an important role during the establishment of the infection and during the life of the parasite inside the parasitophorous vacuole.

show abstract

Cell Surface Heparan Sulfate Promotes Replication of Toxoplasma gondii

Cited by 24 publications

References 55 publications

The Cryptosporidium parvum C-Type Lectin CpClec Mediates Infection of Intestinal Epithelial Cells via Interactions with Sulfated Proteoglycans

The Cryptosporidium parvum C-Type Lectin CpClec Mediates Infection of Intestinal Epithelial Cells via Interactions with Sulfated Proteoglycans

Attachment ofChlamydia trachomatisL2 to host cells requires sulfation

Toxoplasma gondii secretory proteins bind to sulfated heparin structures

Contact Info

Product

Resources

About