Identification of the virulence landscape essential for Entamoeba histolytica invasion of the human colon

PLoS Pathog. 2013;9(12):e1003824. doi: 10.1371/journal.ppat.1003824. Epub 2013 Dec 19.

Abstract

Entamoeba histolytica is the pathogenic amoeba responsible for amoebiasis, an infectious disease targeting human tissues. Amoebiasis arises when virulent trophozoites start to destroy the muco-epithelial barrier by first crossing the mucus, then killing host cells, triggering inflammation and subsequently causing dysentery. The main goal of this study was to analyse pathophysiology and gene expression changes related to virulent (i.e. HM1:IMSS) and non-virulent (i.e. Rahman) strains when they are in contact with the human colon. Transcriptome comparisons between the two strains, both in culture conditions and upon contact with human colon explants, provide a global view of gene expression changes that might contribute to the observed phenotypic differences. The most remarkable feature of the virulent phenotype resides in the up-regulation of genes implicated in carbohydrate metabolism and processing of glycosylated residues. Consequently, inhibition of gene expression by RNA interference of a glycoside hydrolase (β-amylase absent from humans) abolishes mucus depletion and tissue invasion by HM1:IMSS. In summary, our data suggest a potential role of carbohydrate metabolism in colon invasion by virulent E. histolytica.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Amino Acid Sequence
  • Animals
  • Cloning, Molecular
  • Colon / parasitology*
  • Colon / pathology
  • Cricetinae
  • Dysentery, Amebic / genetics
  • Dysentery, Amebic / parasitology*
  • Entamoeba histolytica / genetics
  • Entamoeba histolytica / growth & development*
  • Entamoeba histolytica / pathogenicity*
  • Host-Parasite Interactions / genetics
  • Humans
  • Male
  • Mesocricetus
  • Models, Molecular
  • Molecular Sequence Data
  • Sequence Homology, Amino Acid
  • Virulence Factors / genetics*
  • Virulence Factors / metabolism
  • beta-Amylase / genetics
  • beta-Amylase / metabolism

Substances

  • Virulence Factors
  • beta-Amylase

Grants and funding

This work is supported by grants to NG from the French National Agency for Research (MIE-08). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.