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  • Gal-lectin-dependent contact activates the inflammasome by invasive Entamoeba histolytica.

Gal-lectin-dependent contact activates the inflammasome by invasive Entamoeba histolytica.

Mucosal immunology (2013-11-21)
L Mortimer, F Moreau, S Cornick, K Chadee
ABSTRACT

Entamoeba histolytica (Eh) is an extracellular protozoan parasite of the human colon, which occasionally breaches the intestinal barrier. Eradicating ameba that invades is essential for host survival. A defining but uncharacterized feature of amebic invasion is direct contact between ameba and host cells. This event corresponds with a massive pro-inflammatory response. To date, pathogen recognition receptors (PRRs) that are activated by contact with viable Eh are unknown. Here we show that the innate immune system responds in a qualitatively different way to contact with viable Eh vs. soluble ligands produced by viable or dead ameba. This unique Eh Gal-lectin contact-dependent response in macrophages was mediated by activation of the inflammasome. Soluble native Gal-lectin did not induce inflammasome activation, but was sufficient for transcriptional priming of the inflammasome and non-inflammasome-dependent pro-inflammatory cytokine release. We conclude the inflammasome is a pathogenicity sensor for invasive Eh and identify for the first time a PRR that specifically responds to contact with intact parasites in a manner that accords with scale immune response to parasite invasion.

MATERIALS
Product Number
Brand
Product Description

Galactose, European Pharmacopoeia (EP) Reference Standard
USP
Galactose, United States Pharmacopeia (USP) Reference Standard
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DL-Glyceraldehyde 3-phosphate solution, 45-55 mg/mL in H2O
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Sigma-Aldrich
D-(+)-Galactose, ≥99% (HPLC)
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