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Therap Adv Gastroenterol. 2016 Jan;9(1):37-49. doi: 10.1177/1756283X15616576.

The potential utility of tight junction regulation in celiac disease: focus on larazotide acetate.

Author information

1
Division of Gastroenterology and Hepatology, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA.
2
Professor of Medicine, Division of Gastroenterology and Hepatology, Mayo Clinic, 200 1st St SW, Rochester, MN 55905, USA.

Abstract

Celiac disease (CD) is a common chronic immune disease triggered by gluten. Gliadin peptides pass through the epithelial layers, either paracellularly or transcellularly, to launch a potent adaptive immune response in the lamina propria. This aberrant immune response leads to diverse gastrointestinal and extra-gastrointestinal symptoms. Currently, the only treatment for CD is a strict lifelong adherence to a gluten-free diet (GFD), which can be challenging. An early effect of gluten in CD is an increase in gut permeability. Larazotide acetate, also known as AT-1001, is a synthetic peptide developed as a permeability regulator primarily targeting CD. In vitro studies indicate that larazotide acetate is capable of inhibiting the actin rearrangement caused by gliadin and clinical studies have been conducted using this peptide as a therapy for CD.

KEYWORDS:

Caco-2 cells; gliadin; gluten-free diet; intestinal integrity; paracellular permeability; zonulin

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