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Quantitative proteomics reveals metabolic reprogramming in host cells induced by trophozoites and intermediate subunit of Gal/GalNAc lectins from Entamoeba histolytica

ABSTRACT: The raw proteomics data in the manuscript "Quantitative proteomics reveals metabolic reprogramming in host cells induced by trophozoites and intermediate subunit of Gal/GalNAc lectins from Entamoeba histolytica".

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Xunjia Cheng

PROVIDER: PXD031959 | JPOST Repository | Tue Mar 01 00:00:00 GMT 2022

REPOSITORIES: jPOST

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Dataset's files

Source:

			Action	DRS
	Caco2_Eh.csv	Csv
	Caco2_Igl.csv	Csv
	zl_dia_20210403_cxj_13_Slot2-41_1_5959.d.zip	Other
	zl_dia_20210403_cxj_14_Slot2-41_1_5960.d.zip	Other
	zl_dia_20210403_cxj_15_Slot2-41_1_5961.d.zip	Other

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Project description:Entamoeba histolytica is an intestinal protozoan parasite with remarkable ability to kill and phagocytose host cells, causing amoebic colitis and extraintestinal abscesses. The intermediate subunit (Igl) of galactose (Gal)- and N-acetyl-d-galactosamine (GalNAc)-specific lectins is considered an important surface antigen involved in the pathogenesis of E. histolytica. Here, we applied mass spectrometry-based quantitative proteomics technology to analyze the protein expression profile changes occurring in host Caco2 cells incubated with E. histolytica trophozoites or stimulated by purified native Igl protein. The expression levels of 1,490 and 489 proteins were significantly altered in the E. histolytica-treated and Igl-treated groups, respectively, among 6,875 proteins totally identified. Intriguingly, central carbon metabolism of host cells was suppressed in both E. histolytica-treated and Igl-treated groups, with evidence of decreased expression levels of several key enzymes, including pyruvate kinase muscle type 2, presenting a Warburg-like effect in host cells. Besides, Igl had potential physical interactions with central carbon metabolism enzymes and the proteolytic degradation family members proteasome subunit alpha and beta, which may be responsible for the degradation of key enzymes in carbon metabolism. These results provided a novel perspective on the pathogenic mechanism of E. histolytica and compelling evidence supporting the important role of Igl in the virulence of E. histolytica. IMPORTANCE Metabolic reprogramming is considered a hallmark of some infectious diseases. However, in amoebiasis, a neglected tropical disease caused by protozoan parasite E. histolytica, metabolic changes in host cells have yet to be proven. In this study, advanced data-independent acquisition mass spectrometry-based quantitative proteomics was applied to investigate the overall host cellular metabolic changes as high-throughput proteomics could measure molecular changes in a cell or tissue with high efficiency. Enrichment analysis of differentially expressed proteins showed biological processes and cellular pathways related to amoeba infection and Igl cytotoxicity. Specifically, central carbon metabolism of host cells was dramatically suppressed in both E. histolytica-treated and Igl-treated groups, indicating the occurrence of a Warburg-like effect induced by trophozoites or Igl from E. histolytica. Distinct differences in ubiquitin-mediated proteolysis, rapamycin (mTOR) signaling pathway, autophagy, endocytosis, and tight junctions provided novel perspectives on the pathogenic mechanism of E. histolytica.

Dataset Information

Quantitative proteomics reveals metabolic reprogramming in host cells induced by trophozoites and intermediate subunit of Gal/GalNAc lectins from Entamoeba histolytica

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