Major surface immunogens of Trypanosoma cruzi trypomastigotes

Ouaissi, Ali; Cornette, J.; Taibi, A.; Velge, Philippe; Càpron, André

doi:10.1590/s0074-02761988000500058

Cited by 6 publications

(5 citation statements)

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“…All proteins that display trans-sialidase activity clustered together (TcSgroupI, blue). Another cluster was formed (TcSgroupII, dark green) from TcS proteins that have no trans-sialidase activity but that are capable of binding to β-galactose, laminin [35], fibronectin [36], collagen [37], [38], and cytokeratin [39] and are involved in cell adhesion and invasion. The third TcS group encompasses proteins involved in the regulation of the complement system (CRP - complement regulatory proteins).…”

Section: Discussionmentioning

confidence: 99%

Genomic Analyses, Gene Expression and Antigenic Profile of the Trans-Sialidase Superfamily of Trypanosoma cruzi Reveal an Undetected Level of Complexity

et al. 2011

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The protozoan parasite Trypanosoma cruzi is the etiologic agent of Chagas disease, a highly debilitating human pathology that affects millions of people in the Americas. The sequencing of this parasite's genome reveals that trans-sialidase/trans-sialidase-like (TcS), a polymorphic protein family known to be involved in several aspects of T. cruzi biology, is the largest T. cruzi gene family, encoding more than 1,400 genes. Despite the fact that four TcS groups are well characterized and only one of the groups contains active trans-sialidases, all members of the family are annotated in the T. cruzi genome database as trans-sialidase. After performing sequence clustering analysis with all TcS complete genes, we identified four additional groups, demonstrating that the TcS family is even more heterogeneous than previously thought. Interestingly, members of distinct TcS groups show distinctive patterns of chromosome localization. Members of the TcSgroupII, which harbor proteins involved in host cell attachment/invasion, are preferentially located in subtelomeric regions, whereas members of the largest and new TcSgroupV have internal chromosomal locations. Real-time RT-PCR confirms the expression of genes derived from new groups and shows that the pattern of expression is not similar within and between groups. We also performed B-cell epitope prediction on the family and constructed a TcS specific peptide array, which was screened with sera from T. cruzi-infected mice. We demonstrated that all seven groups represented in the array are antigenic. A highly reactive peptide occurs in sixty TcS proteins including members of two new groups and may contribute to the known cross-reactivity of T. cruzi epitopes during infection. Taken together, our results contribute to a better understanding of the real complexity of the TcS family and open new avenues for investigating novel roles of this family during T. cruzi infection.

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Section: Discussionmentioning

confidence: 99%

Genomic Analyses, Gene Expression and Antigenic Profile of the Trans-Sialidase Superfamily of Trypanosoma cruzi Reveal an Undetected Level of Complexity

et al. 2011

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“…Minimal trans -sialidase activity was detected in amastigotes [ 61 ]. Trans -Sialidase is known to be involved in trypomastigote cell adhesion and invasion process by interacting with a wide range of ligands, such as laminin, fibronectin, and collagen [ 62 – 65 ]. Inhibition of T. cruzi trans -sialidase by specific antibodies led to the increased rate of infection [ 66 ].…”

Section: T Cruzi Infection and Host Cholesteromentioning

confidence: 99%

Trypanosoma cruziInfection and Host Lipid Metabolism

Miao

Ndao

2014

Mediators of Inflammation

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Trypanosoma cruzi is the causative agent of Chagas disease. Approximately 8 million people are thought to be affected worldwide. Several players in host lipid metabolism have been implicated in T. cruzi-host interactions in recent research, including macrophages, adipocytes, low density lipoprotein (LDL), low density lipoprotein receptor (LDLR), and high density lipoprotein (HDL). All of these factors are required to maintain host lipid homeostasis and are intricately connected via several metabolic pathways. We reviewed the interaction of T. cruzi with each of the relevant host components, in order to further understand the roles of host lipid metabolism in T. cruzi infection. This review sheds light on the potential impact of T. cruzi infection on the status of host lipid homeostasis.

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“…The gp85/trans-sialidases are not expressed by the noninfective epimastigote form of T.cruzi . There are approximately 700 gp85/trans-sialidase genes and equal amounts of pseudogenes, in the parasite genome of T. cruzi , Cl Brener strain [7] and the proteins encoded by this supergene family are believed to participle in parasite host cell adhesion and invasion by interacting with multiple ligands, such as laminin [8] , fibronectin [9] , collagen [10] , [11] , cytokeratin (CK) [12] and probably, other cell surface and extracellular proteins [1] . Members of the gp85/trans-sialidase family share a signature conserved sequence (VTVxNVxLYNR) upstream from the carboxyl terminus [13] , [14] .…”

Section: Introductionmentioning

confidence: 99%

Role of the gp85/Trans-Sialidases in Trypanosoma cruzi Tissue Tropism: Preferential Binding of a Conserved Peptide Motif to the Vasculature In Vivo

et al. 2010

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BackgroundTransmitted by blood-sucking insects, the unicellular parasite Trypanosoma cruzi is the causative agent of Chagas' disease, a malady manifested in a variety of symptoms from heart disease to digestive and urinary tract dysfunctions. The reasons for such organ preference have been a matter of great interest in the field, particularly because the parasite can invade nearly every cell line and it can be found in most tissues following an infection. Among the molecular factors that contribute to virulence is a large multigene family of proteins known as gp85/trans-sialidase, which participates in cell attachment and invasion. But whether these proteins also contribute to tissue homing had not yet been investigated. Here, a combination of endothelial cell immortalization and phage display techniques has been used to investigate the role of gp85/trans-sialidase in binding to the vasculature.MethodsBacteriophage expressing an important peptide motif (denominated FLY) common to all gp85/trans-sialidase proteins was used as a surrogate to investigate the interaction of this motif with the endothelium compartment. For that purpose phage particles were incubated with endothelial cells obtained from different organs or injected into mice intravenously and the number of phage particles bound to cells or tissues was determined. Binding of phages to intermediate filament proteins has also been studied.Findings and ConclusionsOur data indicate that FLY interacts with the endothelium in an organ-dependent manner with significantly higher avidity for the heart vasculature. Phage display results also show that FLY interaction with intermediate filament proteins is not limited to cytokeratin 18 (CK18), which may explain the wide variety of cells infected by the parasite. This is the first time that members of the intermediate filaments in general, constituted by a large group of ubiquitously expressed proteins, have been implicated in T. cruzi cell invasion and tissue homing.

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Major surface immunogens of Trypanosoma cruzi trypomastigotes

Cited by 6 publications

References 0 publications

Genomic Analyses, Gene Expression and Antigenic Profile of the Trans-Sialidase Superfamily of Trypanosoma cruzi Reveal an Undetected Level of Complexity

Genomic Analyses, Gene Expression and Antigenic Profile of the Trans-Sialidase Superfamily of Trypanosoma cruzi Reveal an Undetected Level of Complexity

Trypanosoma cruziInfection and Host Lipid Metabolism

Role of the gp85/Trans-Sialidases in Trypanosoma cruzi Tissue Tropism: Preferential Binding of a Conserved Peptide Motif to the Vasculature In Vivo

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