Dataset Information

Comparative proteomics of Trypanosoma cruzi Y and VFRA strains.

ABSTRACT: Chagas disease is one of the most lethal diseases in Latin America, but currently it has become a global health problem because of migration. It is caused by the parasite Trypanosoma cruzi (T. cruzi), an intracellular flagellated protist whose life cycle has been defined in detail, although the immunopathology of its infection is still quite unknown. Moreover, there are differences in pathogenicity between the strains in mice, Y produces a high lethality while VFRA remains in the host in a most chronic manner. Comparative proteomics studies between T. cruzi strains have not been performed extensively, they should allow the detection of relevant virulent factors or distinctive functions. We focused on the proteome analysis of trypomastigotes of Y and VFRA strains by mass spectrometry followed by gene ontology analysis to display similarities or differences in cellular components, biological processes and molecular functions. Also, we performed metabolic pathways enrichment analysis to see the most relevant pathways in each strain. There were a 20% of different proteins showing that Y strain has specific proteins for replication and growth, while VFRA for localization or transport, among others. We found a very similar profile in the different ontology groups, but with some punctual differences. We detected enriched antioxidant defenses in VFRA that could correlate with its behavior of chronic infection in mice controlling the ROS production, while Y strain displayed a great enrichment of pathways related with nucleotides and protein production, explaining the high parasite load and lethality of this strain.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Trypanosoma Cruzi

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Chagas Disease

SUBMITTER: Alfonso Herreros Cabello

LAB HEAD: Núria Gironès and Manuel Fresno

PROVIDER: PXD012536 | Pride | 2019-09-25

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	VFRA_Strain_Replicate_1.msf	Msf
	VFRA_Strain_Replicate_1.raw	Raw
	VFRA_Strain_Replicate_2.msf	Msf
	VFRA_Strain_Replicate_2.raw	Raw
	Y_Strain_Replicate_1.msf	Msf

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Publications

Comparative proteomic analysis of trypomastigotes from Trypanosoma cruzi strains with different pathogenicity.

Herreros-Cabello Alfonso A Callejas-Hernández Francisco F Fresno Manuel M Gironès Núria N

Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases 20190916

Chagas disease, caused by the parasite Trypanosoma cruzi, is one of the most neglected diseases in Latin America, being currently a global health problem. Its immunopathogenesis is still quite unknown. Moreover, there are important differences in pathogenicity between some different T. cruzi strains. For example, in mice, Y strain produces a high acute lethality while VFRA remains in the host mostly in a chronic manner. Comparative proteomic studies between T. cruzi strains represent a complemen ...[more]

PMID: 31536808

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Project description:To investigate the early host response triggered by three different strains of Trypanosoma cruzi at a local infection site, changes in host gene expression were monitored in a murine intradermal infection model using Affymetrix oligonucleotide arrays. Robust induction of IFN-stimulated genes (ISGs) was observed in excised skin 24 hours post-infection where the level of ISG induction was parasite strain-dependent with the least virulent strain triggering a muted IFN response. Infection of mice immunodepleted of IFNÎ³-producing cells or infection of IFNÎ³-deficient mice had minimal impact on the IFN response generated in T. cruzi infected mice. In contrast, infection of mice lacking the type I IFN receptor demonstrated that type I IFNs are largely responsible for the IFN response generated at the site of infection. These data highlight type I IFNs as important components of the innate immune response to T. cruzi the site of inoculation and their role in shaping the early transcriptional response to this pathogen. We used microarrays to detail the local host transcriptional response to intradermal T. cruzi infection in WT mice and mice depleted of NK cells, or deficient in IFN-gamma or type I IFN responses. Additionally we compared the local host-transcriptional response generated to infection with 3 different strains of Trypanosoma cruzi (Y, Brazil, and G). Experiment Overall Design: Mice were infected by intradermal injection of 10^6 T. cruzi trypomastigotes in 100uL of saline split between 2 adjacent sites on the shaved side flank. Control mice were injected with an equal volume of saline. 24 hours post-injection approximately 75mm^2 of skin immediately surrounding the injection site was excised and RNA was isolated from the tissue. Balb/c mice were used for most experiments and IFN-gamma KO mice were on the Balb/c background. WT 129 mice were also used as IFNAR-/- mice were on the 129 background. In total 33 arrays were performed. 7 WT (Balb/c) control, 3 Y strain infected, 3 Brazil strain infected, 3 G strain infected, 2 IFN-gamma KO control, 2 IFN-gamma KO infected, 1 NK cell depleted control, 1 NK cell depleted infected, 3 WT (129) control, 3 WT (129) infected, 3 IFNAR KO control, 3 IFNAR KO infected