Abstract

Celiac Disease (also known as gluten‐sensitive enteropathy and nontropical sprue) is estimated to affect between 0.5–1.0% of the general population of the United States (1.6 million to 3.3 million during 2017) with many of these cases being under‐diagnosed. Celiac Disease (CD) is the genetic hypersensitivity to ingested exogenous gluten. Subsequent exposure to gluten related proteins lead to the development of an autoimmune response, causing damage to the lining of the gastrointestinal tract. Due to increased inflammation, symptomatic individuals present with abdominal pain, diarrhea, nausea, and many other gastrointestinal complications. However, some individuals affected by CD are asymptomatic creating increased diagnostic error. An accurate diagnosis of CD remains challenging; current diagnostic procedures involve multi‐day serological screening, followed by invasive gastrointestinal biopsies of suspected lesions. Baring this in mind, there is a pressing need for a rapid, non‐invasive, and accurate detection method to diagnose individuals suffering from this disease. Our method is based on the known autoimmune interactions related to CD. Specifically, we observe the formation of a structured complex between a unique epitope—a chimera of tissue transglutaminase 2 and truncated gluten peptide—and the autoantibodies produced in response to the presence of gluten related proteins. Conducted within our research, we demonstrate a CD‐related diagnostic tool for early, accurate, and rapid disease identification of affected individuals. This tool is a electrochemical DNA‐based biosensor (E‐DNA) that relies on peptide epitopes acting as capture probes to detect levels of disease‐specific antibodies. This commonly used biosensor is utilized to detect small changes in electrical conductivity to determine whether or not a target molecule has been bound. In principle, this sensor design can be utilized for unprocessed finger‐lancet blood samples to provide a rapid digital readout, allowing for efficient and accurate diagnoses of CD affected patients.Support or Funding InformationThis work is supported by internal grant funding from the Metropolitan State University of Denver.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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