Dataset Information

Testis proteome of Trypanosoma cruzi infected mice

ABSTRACT: Male CD-1 mice (N=8) were intraperitoneally infected by culture-derived Trypanosoma cruzi trypomastigotes of the Brazil strain. One group (N=4) was treated with an antitrypanosomal drug (nifurtimox) on day 74 post-infection (chronic phase) for 20 days. A group of uninfected mice (N=3) was also included as control. All groups (N=11) were enthanized on day 110 post-infection, testes were collected and subjected to 2D-LC-MS/MS analysis. Label-free quantitation revealed that the testes of T. cruzi-infected mice had an altered proteome pattern relative to treated mice and uninfected controls. The analysis also demonstrated that the left and right testes had different proteomic profiles in infected animals.

INSTRUMENT(S): maXis

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Testis

DISEASE(S): Trypanosomiasis

SUBMITTER: Momar Ndao

LAB HEAD: Momar Ndao

PROVIDER: PXD017802 | Pride | 2023-03-10

REPOSITORIES: Pride

ACCESS DATA

Publications

New metabolic signature for Chagas disease reveals sex steroid perturbation in humans and mice.

Golizeh Makan M Nam John J Chatelain Eric E Jackson Yves Y Ohlund Leanne B LB Rasoolizadeh Asieh A Camargo Fabio Vasquez FV Mahrouche Louiza L Furtos Alexandra A Sleno Lekha L Ndao Momar M

Heliyon 20221215 12

The causative agent of Chagas disease (CD), <i>Trypanosoma cruzi</i>, claims thousands of lives each year. Current diagnostic tools are insufficient to ensure parasitological detection in chronically infected patients has been achieved. A host-derived metabolic signature able to distinguish CD patients from uninfected individuals and assess antiparasitic treatment efficiency is introduced. Serum samples were collected from chronic CD patients, prior to and three years after treatment, and subjec ...[more]

PMID: 36590505

Similar Datasets

Project description:The major inducible 70 kDa heat shock protein (hsp70) is host protective in a mouse model of measles virus (MeV) brain infection. Transgenic constitutive expression of hsp70 in neurons, the primary target of MeV infection, abrogates neurovirulence in neonatal H-2d congenic C57BL/6 mice. A significant level of protection is retained after depletion of T lymphocytes, implicating innate immune mechanisms. Focus of the present work was to elucidate the basis for hsp70-dependent innate immunity using this model. Transcriptome analysis of brains from transgenic (TG) and non-transgenic (NT) mice 5 days after infection identified type 1 interferon (IFN) signaling and macrophage activation/antigen presentation as the main differences linked to survival. The pivotal role for type 1 IFN in hsp70-mediated protection was demonstrated in mice with a genetically disrupted type 1 IFN receptor (IFNAR-/-), where IFNAR-/- eliminated the difference in survival between TG and NT mice. Brain macrophages, not neurons, are the predominant source of type 1 IFN in the virus-infected brain, and in vitro studies provided a mechanistic basis by which MeV-infected neurons can induce IFN-β in uninfected microglia in an hsp70-dependent manner. MeV infection induced extracellular release of hsp70 from mouse neuronal cells that constitutively express hsp70, and extracellular hsp70 induced IFN-β transcription in mouse microglial cells through Toll-like receptors 2 and 4. Collectively, results support a novel axis of type 1 IFN-dependent antiviral immunity in the virus-infected brain that is driven by hsp70. Hsp70 expression in mice enhances gene expression related to antiviral immune response against MeV neurovirulence. We performed microarrays on whole brain tissues in mice to obtain an unbiased picture of how hsp70 alters host innate responses to viral infection. Hsp70-overexpressing transgenic (TG) and non-transgenic (NT) mice were infected with MeV intracranially, and total brain mRNA harvested at 5 and 10 days post infection (d.p.i.) was analyzed, sampling the hemisphere opposite the side of viral inoculation. Analysis includes 6 groups: infected TG at 5 d.p.i. (n=4), infected TG at 10 d.p.i. (n=5), infected NT at 5 d.p.i. (n=4), infected NT at 10 d.p.i. (n=5), uninfected TG at 5 d.p.i. (n=4), and uninfected NT at 5 d.p.i. (n=4).

Dataset Information

Testis proteome of Trypanosoma cruzi infected mice

Publications

New metabolic signature for Chagas disease reveals sex steroid perturbation in humans and mice.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure