Microvesicles released from Giardia intestinalis disturb host-pathogen response in vitro

Ingrid Evans-Osses, Andres Mojoli, Marta Monguió-Tortajada, Antonio Marcilla, Veronica Aran, Maria Amorim, Jameel Inal, Francesc E Borràs, Marcel I Ramirez

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)
48 Downloads (Pure)


Giardia intestinalis (G.I), is an anaerobic protozoan and the aetiological agent of giardiasis, a diarrhoea present worldwide and associated with poverty. G.I has a simple life cycle alternating between cyst and trophozoite. Cysts are transmitted orally to the stomach and transform to trophozoites in the intestine by a multifactorial process. Recently, microvesicles (MVs) have been found to be released from a wide range of eukaryotic cells. We have observed a release of MVs during the life cycle of G.I., identifying MVs from active trophozoites and from trophozoites differentiating to the cyst form. The aim of the current work was to investigate the role of MVs from G.I in the pathogenesis of giardiasis. MVs from log phase were able to increase the attachment of G. intestinalis trophozoites to Caco-2 cells. Moreover, MVs from G. intestinalis could be captured by human immature dendritic cells, resulting in increased activation and allostimulation of human dendritic cells. Lipid rafts participate in the MV biogenesis and in the attachment to Caco-2 cells. Nevertheless, proteomic analysis from two types of MVs has shown slight differences at the protein levels. An understanding of biogenesis and content of MVs derived from trophozoites might have important implications in the pathogenesis of the disease.

Original languageEnglish
Pages (from-to)131-142
Number of pages12
JournalEuropean Journal of Cell Biology
Issue number2
Early online date22 Jan 2017
Publication statusPublished - 31 Mar 2017


  • Animals
  • Caco-2 Cells
  • Cell-Derived Microparticles
  • Extracellular Vesicles
  • Giardia lamblia
  • Giardiasis
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Innate
  • Journal Article


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