scholarly journals Excreted Trypanosoma brucei proteins inhibit Plasmodium hepatic infection

2021 ◽  
Vol 15 (10) ◽  
pp. e0009912
Author(s):  
Adriana Temporão ◽  
Margarida Sanches-Vaz ◽  
Rafael Luís ◽  
Helena Nunes-Cabaço ◽  
Terry K. Smith ◽  
...  
Keyword(s):  
Trypanosoma Brucei ◽  
Protein S ◽  
Surface Glycoprotein ◽  
Common Disease ◽  
Defence Mechanism ◽  
Trypanosome Infection ◽  
Protein Excretion ◽  
Biochemical Characterisation ◽  
Liver Infection ◽  
Malaria Severity

Malaria, a disease caused by Plasmodium parasites, remains a major threat to public health globally. It is the most common disease in patients with sleeping sickness, another parasitic illness, caused by Trypanosoma brucei. We have previously shown that a T. brucei infection impairs a secondary P. berghei liver infection and decreases malaria severity in mice. However, whether this effect requires an active trypanosome infection remained unknown. Here, we show that Plasmodium liver infection can also be inhibited by the serum of a mouse previously infected by T. brucei and by total protein lysates of this kinetoplastid. Biochemical characterisation showed that the anti-Plasmodium activity of the total T. brucei lysates depends on its protein fraction, but is independent of the abundant variant surface glycoprotein. Finally, we found that the protein(s) responsible for the inhibition of Plasmodium infection is/are present within a fraction of ~350 proteins that are excreted to the bloodstream of the host. We conclude that the defence mechanism developed by trypanosomes against Plasmodium relies on protein excretion. This study opens the door to the identification of novel antiplasmodial intervention strategies.

scholarly journals Synchronous expression of individual metacyclic variant surface glycoprotein genes in Trypanosoma brucei

2015 ◽  
Vol 200 (1-2) ◽  
pp. 1-4 ◽  
Author(s):  
Kiantra Ramey-Butler ◽  
Elisabetta Ullu ◽  
Nikolay G. Kolev ◽  
Christian Tschudi
Keyword(s):  
Trypanosoma Brucei ◽  
Surface Glycoprotein ◽  
Variant Surface Glycoprotein

Trypanosome infections and survival in tsetse

Parasitology ◽  
1998 ◽  
Vol 116 (S1) ◽  
pp. S23-S28 ◽  
Author(s):  
I. Maudlin ◽  
S. C. Welburn ◽  
P. J. M. Milligan
Keyword(s):  
Salivary Gland ◽  
Salivary Glands ◽  
Trypanosoma Brucei ◽  
Glossina Morsitans Morsitans ◽  
Trypanosoma Congolense ◽  
Vectorial Capacity ◽  
Trypanosome Infection ◽  
Trypanosoma Brucei Rhodesiense ◽  
Glossina Morsitans ◽  
Differential Effects

SummaryThe effect of trypanosome infection on vector survival was observed in a line of Glossina morsitans morsitans selected for susceptibility to trypanosome infection. The differential effects of midgut and salivary gland infections on survival were examined by exposing flies to infection with either Trypanosoma congolense which colonizes midgut and mouthparts or Trypanosoma brucei rhodesiense which colonizes midgut and salivary glands. A comparison of the survival distributions of uninfected flies with those exposed to infection showed that salivary gland infection significantly reduces tsetse survival; midgut infection had little or no effect on the survival of tsetse. The significance of these findings is discussed in relation to the vectorial capacity of wild flies.

scholarly journals Differential regulation of two distinct families of glucose transporter genes in Trypanosoma brucei.

1993 ◽  
Vol 13 (2) ◽  
pp. 1146-1154 ◽  
Author(s):  
F Bringaud ◽  
T Baltz
Keyword(s):  
Trypanosoma Brucei ◽  
Xenopus Oocytes ◽  
Glucose Transporter ◽  
Protein S ◽  
Life Cycle Stage ◽  
Good Target ◽  
Hexose Transporters ◽  
Moderate Sensitivity ◽  
Mrna Analysis

A tandemly arranged multigene family encoding putative hexose transporters in Trypanosoma brucei has been characterized. It is composed of two 80% homologous groups of genes called THT1 (six copies) and THT2 (five copies). When Xenopus oocytes are microinjected with in vitro-transcribed RNA from a THT1 gene, they express a glucose transporter with properties similar to those of the trypanosome bloodstream-form protein(s). This THT1-encoded transport system for glucose differs from the human erythrocyte-type glucose transporter by its moderate sensitivity to cytochalasin B and its capacity to transport D-fructose. These properties suggest that the trypanosomal transporter may be a good target for antitrypanosomal drugs. mRNA analysis revealed that expression of these genes was life cycle stage dependent. Bloodstream forms express 40-fold more THT1 than THT2. In contrast, procyclic trypanosomes express no detectable THT1 but demonstrate glucose-dependent expression of THT2.

Trypanosoma brucei: posttranscriptional control of the variable surface glycoprotein gene expression site

1989 ◽  
Vol 9 (9) ◽  
pp. 4018-4021
Author(s):  
E Pays ◽  
H Coquelet ◽  
A Pays ◽  
P Tebabi ◽  
M Steinert
Keyword(s):  
Gene Expression ◽  
Trypanosoma Brucei ◽  
Transcription Initiation ◽  
Tsetse Fly ◽  
Surface Glycoprotein ◽  
Insect Vector ◽  
Variable Surface Glycoprotein ◽  
A Genome ◽  
Variable Surface ◽  
Expression Site

The arrest of variable surface glycoprotein (VSG) synthesis is one of the first events accompanying the differentiation of Trypanosoma brucei bloodstream forms into procyclic forms, which are characteristic of the insect vector. This is because of a very fast inhibition of VSG gene transcription which occurs as soon as the temperature is lowered. We report that this effect is probably not controlled at the level of transcription initiation, since the beginning of the VSG gene expression site, about 45 kilobases upstream from the antigen gene, remains transcribed in procyclic forms. The permanent activity of the promoter readily accounts for the systematic reappearance, upon return to the bloodstream form after cyclical transmission, of the antigen type present before passage to the tsetse fly. The abortive transcription of the VSG gene expression site appears linked to RNA processing abnormalities. Such posttranscriptional controls may allow the modulation of gene expression in a genome organized in large multigenic transcription units.

Metacyclic variant surface glycoprotein genes of Trypanosoma brucei subsp. rhodesiense are activated in situ, and their expression is transcriptionally regulated

1986 ◽  
Vol 6 (6) ◽  
pp. 1991-1997
Author(s):  
M J Lenardo ◽  
K M Esser ◽  
A M Moon ◽  
L H Van der Ploeg ◽  
J E Donelson
Keyword(s):  
Trypanosoma Brucei ◽  
Gene Deletion ◽  
Surface Glycoprotein ◽  
Mammalian Host ◽  
Small Subset ◽  
Insect Vector ◽  
Gradient Electrophoresis ◽  
Variant Surface Glycoproteins ◽  
Variant Antigen

During the metacyclic stage in the life cycle of Trypanosoma brucei subsp. rhodesiense, the expression of variant surface glycoproteins (VSGs) is restricted to a small subset of antigenic types. Previously we identified cDNAs for the VSGs expressed in metacyclic variant antigen types (MVATs) 4 and 7 and found that these VSG genes do not rearrange when expressed at the metacyclic stage (M. J. Lenardo, A. C. Rice-Ficht, G. Kelly, K. Esser, and J. E. Donelson, Proc. Nathl. Acad Sci. USA 81:6642-6646, 1984). We now provide further evidence that these genes do not rearrange and demonstrate that their 5' upstream regions lack the 72 to 76-base-pair repeats which are considered the substrate for duplication and transposition events. Pulsed field gradient electrophoresis showed that the MVAT VSG genes were located on the largest chromosome-sized DNA molecules, and the lack of the MVAT 4 gene in one of two different serodemes suggested that one mechanism for the evolution of MVAT repertoires is gene deletion. When MVATs were inoculated into the bloodstream of a mammalian host by a bite from the insect vector, they rapidly switched into nonmetacyclic VSG types. We found that this switch was accomplished by a loss of MVAT RNA concomitant with the loss of metacyclic VSGs. Transcription studies with isolated metacyclic nuclei showed that the MVAT genes were expressed in situ from a single locus and were regulated at the level of transcription.

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