Jefferson Adams is a freelance writer living in San Francisco. His poems, essays and photographs have appeared in Antioch Review, Blue Mesa Review, CALIBAN, Hayden's Ferry Review, Huffington Post, the Mississippi Review, and Slate among others.
He is a member of both the National Writers Union, the International Federation of Journalists, and covers San Francisco Health News for Examiner.com.
The research team was made up of doctors K. Lindfors, T. Blomqvist, K. Juuti-Uusitalo, S. Stenman, J. Venäläinen, M. Mäki and K. Kaukinen. They are associated with the Paediatric Research Centre for the Medical School of the Finland’s University of Tampere, the Department of Peadiatrics, and the Department of Gastroenterology and Alimentary Tract Surgery at Tampere University Hospital, and the Department of Pharmacology and Toxicology of the Finland’s University of Kuopio.
In people with celiac disease, wheat gliadin causes serious intestinal symptoms and damages the small-bowel mucosa. Untreated, this can leave the individual at risk of developing various cancers and numerous associated conditions. Most all of this can be reversed or prevented if detected and treated early enough.
Currently, the only effective treatment for celiac disease is a strict life-long gluten-free diet. However, a 100% gluten-free diet is nearly impossible to maintain, with so many gluten-free products containing trace amounts of gluten. Because of this, people with celiac disease face regular gluten contamination. Also because of this, acceptable alternatives are desirable.
Earlier studies have indicated that probiotic bacteria might be used in sourdough fermentation to induce the hydrolysis of celiac toxic gluten in food manufacturing, and thereby benefit people with celiac disease.
Although several studies have addressed the ability of probiotic bacteria to detoxify gliadin after an extensive incubation period, the team found none that investigated whether various live probiotic bacteria can inhibit gliadin-induced toxic effects directly on epithelial cells.
In this study the team set out to determine whether probiotics Lactobacillus fermentum or Bifidobacterium lactis might block the toxic effects of gliadin in intestinal cell culture conditions.
To assess the degree to which live probiotics were able to block peptic-tryptic digested gliadin-induced degradation of human colon cells Caco-2, the team measured epithelial permeability by transepithelial resistance, actin cytoskeleton arrangements by the extent of membrane ruffling and expression of tight junctional protein ZO-1.
B. lactis inhibited the gliadin-induced increase dose-dependently in epithelial permeability, and, at higher concentrations totally eliminated the gliadin-induced reduction in transepithelial resistance.
That is, B. lactis decreased or eliminated the compromise in cell-wall resistance caused by gliadin. This means that B. lactis overcame the mechanism that gives rise to the decreased cell resistance and the increased permeability that occurs during an adverse reaction to wheat gliadin.
The B. lactis strain also interfered with the creation of membrane ruffles in Caco-2 cells caused by gliadin exposure. Furthermore, it also shielded the tight junctions of Caco-2 cells from the toxic effects of gliadin, as shown by the way in which ZO-1 is expressed.
The researchers concluded that live B. lactis bacteria might achieve partial to full blockage of gliadin toxicity gluten/gliadin-induced damage in the small-intestinal mucosa of people with celiac disease, and that it merits further study concerning its potential as a dietary supplement to guard against any silent damage associated with accidental gluten-contamination in celiac disease.
Clinical and Experimental Immunology, 152: 552–558