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    New Therapy May Mean Less Dietary Restrictions for Celiac Disease Sufferers


    Scott Adams

    Celiac.com 07/01/2006 - Scientists have discovered what may be a successful non-dietary therapy for celiac sprue, an inherited inflammatory disorder of the small intestine that impacts an estimated 1 in 200 people around the world. Two research studies, published in the June issue of Chemistry and Biology, pave the way for clinical testing with an oral enzyme therapy that may prevent the many symptoms and complications of this widespread disease.


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    People with celiac sprue, also called celiac disease, cannot tolerate the protein gluten in their diet. Gluten is present in grains like wheat, barley, and rye. When gluten is ingested by a celiac patient, it sets off an inflammatory reaction that damages the small intestine, leading to malabsorption, an autoimmune-like response, and many other complications. The only effective therapy for celiac disease is complete dietary exclusion of gluten. However, the ubiquitous nature of gluten poses a constant threat to celiacs, and a majority of celiac patients who adopt a restrictive diet still exhibit structural and functional gut abnormalities.

    "Non-dietary therapies that allow celiac patients to safely incorporate low-to-moderate levels of gluten into their daily diet would be of considerable benefit," explains study leader Dr. Chaitan Khosla, from Stanford University and Celiac Sprue Research Foundation. "Having demonstrated earlier that certain types of enzymes can detoxify gluten, our laboratory set out to devise an optimal oral enzyme therapy for celiac sprue by borrowing from nature. In germinating barley seed, gluten serves as a nutritious storage protein that is efficiently digested by enzymes. One enzyme, EP-B2, plays a crucial role in this process by breaking gluten proteins after glutamine residues, which comprise one-third of all amino acid residues in gluten."

    Dr. Khoslas group used recombinant bacteria to produce a form of EP-B2 that only activates under acidic conditions similar to the conditions found in the human stomach. The researchers demonstrated that EP-B2 efficiently digested gluten protein under gastric conditions and, importantly, EP-B2 was most specific for those parts of gluten that are known to trigger celiac pathogenesis. In a second study, the researchers went on to devise an even more potent double enzyme therapy for detoxifying gluten.

    EP-B2 was tested in combination with another well-characterized enzyme called PEP that breaks gluten protein after proline residues. Like glutamine, proline is also abundant in inflammatory gluten peptides. At very high gluten loads, where neither PEP nor EP-B2 alone could detoxify gluten quickly enough to prevent inflammation, a PEP and EP-B2 combination completely abolished gluten immunotoxicity within ten minutes under simulated gastric and duodenal conditions.

    In this tag-team therapy, EP-B2 first cleaved gluten into small pieces under gastric conditions that were then easier for PEP to fully detoxify under duodenal conditions. "Our results suggest that recombinant EP-B2 should be effective as supportive therapy to help celiacs cope with the hidden gluten in everyday life, and that a two-enzyme cocktail containing PEP and EP-B2 may even allow celiacs to resume a more normal diet in the future," offers Dr. Khosla.

    References:

    Seigel et al.

    The researchers include Matthew Siegel, Michael T. Bethune, Jiang Xia, Alexandre Johannsen, Tor B. Stuge, and Peter P. Lee of Stanford University in Stanford, CA; Jonathan Gass, Jennifer Ehren, Gary M. Gray, and Chaitan Khosla of Stanford University in Stanford, CA and Celiac Sprue Research Foundation in Palo Alto, CA. This research was supported by a grant from the National Institutes of Health (R01 DK63158 to C.K. and Mary Hewitt Loveless, MD Pilot-Project Grant to P.P.L.).

    Siegel et al.: "Rational Design of Combination Enzyme Therapy for Celiac Sprue." Publishing in Chemistry & Biology 13, 649–658, June 2006 DOI 10.1016/j.chembiol.2006.04.009 www.chembiol.com

    Bethune et al.

    The researchers include Michael T. Bethune, Yinyan Tang, and Chaitan Khosla of Stanford University in Stanford, CA; Pavel Strop of Howard Hughes Medical Institute and Stanford University in Stanford, CA; Ludvig M. Sollid of University of Oslo and Rikshospitalet University Hospital in Oslo, Norway. This research was supported by R01 DK063158 to C.K. M.T.B. is a recipient of a National Institutes of Health Cellular and Molecular Biology Training Grant through Stanford University.

    Bethune et al.: "Heterologous Expression, Purification, Refolding, and Structural-Functional Characterization of EP-B2, a Self-Activating Barley Cysteine Endoprotease." Publishing in Chemistry & Biology 13, 637–647, June 2006 DOI 10.1016/j.chembiol.2006.04.008 www.chembiol.com.

    Contact: Heidi Hardman
    Tel: (617) 397-2879

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    Guest Christine

    Posted

    Please, Bring it on, we will try anything just to eat again.... The article of research was in 2006 it is 2009 What happen?

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  • About Me

    In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I founded The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.

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    Scott Adams
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    Dr. Ron Hoggan, Ed.D.
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    References:
    Kuitunen P, Savilahti E, Verkasalo M. Late mucosalrelapse in a boy with coeliac disease and cows milk allergy.Acta Paediatr Scand.1986 Mar;75(2):340-2. Bardella MT, Fredella C, Trovato C, Ermacora E, Cavalli R, Saladino V, Prampolini L. Long-term remission in patients with dermatitis herpetiformis on a normal diet. Br. J. Dermatol. 2003 Nov;149(5):968-71. Shmerling DH, Franckx J. Childhood celiac disease: a long-term analysis of relapses in 91 patients.J Pediatr Gastroenterol Nutr. 1986 Jul-Aug;5(4):565-9. Chartrand LJ, Seidman EG. Celiac disease is a lifelong disorder. Clin Invest Med. 1996 Oct;19(5):357-61. Rostami K, Kerckhaert J, von Blomberg BM, Meijer JW, Wahab P, Mulder CJ. SAT and serology in adult coeliacs, seronegative coeliac disease seems a reality.Neth J Med. 1998 Jul;53(1):15-9. Hudson DA, Cornell HJ, Purdham DR, Rolles CJ. Non-specific cytotoxicity of wheat gliadin components towards cultured human cells.Lancet. 1976 Feb 14;1(7955):339-41.

    Gryphon Myers
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    The study's facilitators began their restrospective analysis by collecting serum samples from 268 patients at hospitals throughout Switzerland, Germany and Austria. All included patients suffered from celiac-like symptoms and underwent both biopsy and antibody testing within 2 months of serum collection. All included patients were on gluten-containing diets at the time of testing. 149 of the patients were ultimately diagnosed with celiac disease; the other 119 showed normal intestinal mucosa and were considered celiac-free. These patients were the control group.
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    http://www.biomedcentral.com/1471-230X/13/19

    Jefferson Adams
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    Source:
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