Dataset Information

Proteomic analysis of the membrane-enriched fraction of trypomastigostes released from wild type, LAMP1/2 KO or LAMP2 KO fibroblasts

ABSTRACT: Trypanosoma cruzi invades non-professional phagocytic cells by subverting their membrane repair process, which is dependent on membrane injury and cell signaling, intracellular calcium increase and lysosome recruitment. Cells lacking Lysosome Associated Membrane Proteins 1 and 2 are less permissive to parasite invasion, however more prone to parasite intracellular multiplication. Several passages through a different intracellular environment can significantly change T. cruzi’s gene expression profile. We evaluated whether one single passage through LAMP deficient (KO) or wild type (WT) fibroblasts could influence invasion ability of T. cruzi Y strain trypomastigotes in L6 myoblasts and WT fibroblasts. Our results regarding their biological behavior clearly indicated that parasites released from WT cells (TcY-WT), LAMP1/2 KO cells (TcY-L1/2-/-) or LAMP2 KO (TcY-L2-/-) cells are distinct from each other. Since these alterations most likely would reflect differences among parasite surface molecules, we also evaluated their proteome. We identified few protein complexes, membrane and secreted proteins regulated in our dataset. Among those, some members of MASP, mucins, trans-sialidases and gp63 proteins family, which are known to play an important role during parasite infection and could correlate to TcY-WT, TcY-L1/2-/- and TcY-L2-/- biological behavior.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Trypanosoma Cruzi

TISSUE(S): Cell Culture

SUBMITTER: Anny Carolline Silva Oliveira

LAB HEAD: Luciana de Oliveira Andrade

PROVIDER: PXD028897 | Pride | 2022-02-17

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	MembFracYstrain.msf	Msf
	MembFracYstrain.msfView	Msf
	MembFracYstrain.pdResult	Other
	MembFracYstrain.pdResultView	Other
	MembFracYstrain_PSMs.txt	Txt

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Publications

Biological and Molecular Effects of Trypanosoma cruzi Residence in a LAMP-Deficient Intracellular Environment.

Oliveira Anny Carolline Silva ACS Rezende Luisa L Gorshkov Vladimir V Melo-Braga Marcella Nunes MN Verano-Braga Thiago T Fernandes-Braga Weslley W Guadalupe Jorge Luís de Melo JLM de Menezes Gustavo Batista GB Kjeldsen Frank F de Andrade Hélida Monteiro HM Andrade Luciana de Oliveira LO

Frontiers in cellular and infection microbiology 20220106

Trypanosoma cruzi invades non-professional phagocytic cells by subverting their membrane repair process, which is dependent on membrane injury and cell signaling, intracellular calcium increase, and lysosome recruitment. Cells lacking lysosome-associated membrane proteins 1 and 2 (LAMP1 and LAMP2) are less permissive to parasite invasion but more prone to parasite intracellular multiplication. Several passages through a different intracellular environment can significantly change T. cr ...[more]

PMID: 35071040

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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

Dataset Information

Proteomic analysis of the membrane-enriched fraction of trypomastigostes released from wild type, LAMP1/2 KO or LAMP2 KO fibroblasts

Dataset's files

Publications

Biological and Molecular Effects of <i>Trypanosoma cruzi</i> Residence in a LAMP-Deficient Intracellular Environment.

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