Toll-like Receptor Signaling Activation by Entamoeba histolytica Induces Beta Defensin 2 in Human Colonic Epithelial Cells: Its Possible Role as an Element of the Innate Immune Response


Por: Ayala-Sumuano, JT, Téllez-López V.M., Dominguez-Robles, MD, Shibayama-Salas M., Meza I.

Publicada: 1 feb 2013
Resumen:
Background: Entamoeba histolytica, a protozoan parasite of humans, produces dysenteric diarrhea, intestinal mucosa damage and extraintestinal infection. It has been proposed that the intestinal microbiota composition could be an important regulatory factor of amebic virulence and tissue invasion, particularly if pathogenic bacteria are present. Recent in vitro studies have shown that Entamoeba histolytica trophozoites induced human colonic CaCo2 cells to synthesize TLR-2 and TLR-4 and proinflammatory cytokines after binding to the amebic Gal/GalNac lectin carbohydrate recognition domain. The magnitude of the inflammatory response induced by trophozoites and the subsequent cell damage were synergized when cells had previously been exposed to pathogenic bacteria. Methodology/Principal Findings: We show here that E. histolytica activation of the classic TLR pathway in CaCo2 cells is required to induce beta defensin-2 (HBD2) mRNA expression and production of a 5-kDa cationic peptide with s

Filiaciones:
Téllez-López V.M.:
 Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, México DF, Mexico

Shibayama-Salas M.:
 Department of Infectomics and Molecular Pathogenesis, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, México DF, Mexico

Meza I.:
 Department of Molecular Biomedicine, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, México DF, Mexico
ISSN: 19352727
Editorial
PUBLIC LIBRARY SCIENCE, 185 BERRY ST, STE 1300, SAN FRANCISCO, CA 94107 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 7 Número: 2
Páginas:
WOS Id: 000315644900043
ID de PubMed: 23469306
imagen All Open Access, Gold

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