NATIONAL RESEARCH & DEVELOPMENT INSTITUTE FOR BIOLOGY AND ANIMAL NUTRITION ROLE OF ENRICHED CALCIUM AND IRON YEASTS IN COELIAC DISEASE MARIN D.E. 1, DUTA.

Slides:



Advertisements
Similar presentations
Celiac Disease This session introduces you to the intestinal malady known as celiac disease or celiac sprue. There are three reasons for looking at this.
Advertisements

The “Great Mimic” Disease
A.M. Report 5/5/09 Jason Haag, M.D.
Definition. Celiac disease is an immune-mediated enteropathycaused by a permanent sensitivity to gluten in genetically susceptible individuals. It occurs.
Celiac disease Prepared by :Maha Hmeidan nahal.
NOVEL ASPECTS IN THE GENETICS OF CELIAC DISEASE: COPY NUMBER VARIATION, METHYLATION AND COREGULATION IN NF  B-RELATED GENES Nora Fernandez Jimenez Doctoral.
Diet and Autoimmune Disease Danielle DeSalvo. Autoimmune Diseases Characterized by an over active immune reaction in which the body attacks it’s own tissues.
“Sprue” is a somewhat antiquated term referring generally to intestinal malabsorption.
Dr Nader Ghaderi, GPR. General information First described in ancient Greek by Aretaeus of Cappadocia The word Coeliac was first used in 19 th century.
SCREENING FOR CELIAC DISEASE IN EGYPTIAN CHILDREN SCREENING FOR CELIAC DISEASE IN EGYPTIAN CHILDREN Prof. Dr: Mona Abu Zekry -Professor of Pediatrics Head.
 An autoimmune disease where the protein gluten damages the villi in the small intestine causing malabsorption.  Celiac Disease is a lifelong condition.
Eat to Heal... the Cure is Food!. Overview  Celiac Disease Definition Symptoms and presentations Diagnosis Treatment  The Kogan Celiac Center at Barnabas.
MALABSORPTION SYNDROME
Lower Gastrointestinal Tract KNH 411. © 2007 Thomson - Wadsworth.
Classifications of Gluten Sensitivity Defining Celiac Disease Grace Coughlan Taylor Nicholson.
Slyter Nutrition Consulting Services
Presentation by Margaret Roberts.  First described in 1880  Link to diet was not described until 1950  In 1954, Dr. Paulley showed that intestinal.
Coeliac Disease Jaide Brown Breea Buckley Krissy Rowe.
1 Meeting Children’s Special Food and Nutrition Needs in Child Nutrition Programs Lesson 5: Managing Celiac Disease.
Katelyn Quealy Morrison Chartwells Dietetic Intern
Lecture 7c 27 February ADEK ABSORPTION AND TRANSPORT carriers for both absorption and transport transport-lipoproteins in the blood.
Lower Gastrointestinal Tract KNH 411. © 2007 Thomson - Wadsworth.
My Dietary Related Disease that I have chosen is: Coeliac Disease.
Celiac Diet By: Alisha Gross, Caitlin Fortenberry, Susie Mays.
Chapter 3 Preconception Nutrition Conditions and Interventions
Gluten Free Diet Accommodating the Gluten Free Diet in The PCH Setting.
In Vitro Gliadin Challenge: Diagnostic Accuracy and Utility for the Difficult Diagnosis of Celiac Disease Am J Gastroenterol 2012; 107:111–117; Raffaella.
APPLIED RESEARCHES CONCERNING THE FORTIFIED GLUTEN-FREE CEREAL-BASED PRODUCTS DESIGN Duta, D.E. 1, Gagiu, V. 1, Olteanu, M. 2 1 Institute of Food Bioresources,
Chronic Diarrheal Diseases Mohammed al-matrafi. Diarrhea more than 2 weeks.
4. Department of Psychiatry, Johns Hopkins School of Medicine
DC-SIGN/HLA-DR+ cells increased in coeliac duodenum 1. Immunology Lab, Dept of Paediatrics & Immunology, University of Valladolid, IBGM-CSIC, Spain; 2.
NUTRITION IN LYME and TICK INFECTIONS Martin D. Fried, MD, FAAP, ABPNS Physician Nutrition Specialist 3200 Sunset Ave Suite 100 Ocean, NJ
THE IMPORTANCE OF DIAGNOSIS AND DIET THERAPY IN CELIAC DISEASE Author: Miklos Andreea Doriana Coordinator: Lecturer dr. Fárr Ana-Maria.
Celiac Disease.
Keogh Institute for Medical Research Coeliac disease – a silent cause of bone loss in midlife 1. Keogh Institute for Medical Research; 2. Department of.
Aramark Dietetic Internship Erika Stahl. Title: Celiac Disease and the Gluten-Free Diet: The Need for Registered Dietitians with Certified Expertise Emerging.
EGF and L-Glutamine Accelerates the Restoration of Epithelial Barrier Function From Oxidative Stress- Induced Injury Nichole Barnhart.
Tissue Transglutaminase, Endomysial Antibodies, and Celiac Disease
Celiac Disease Research Honors Experience Dan Geiser Nov 8th-Dec 2nd.
What is Anemia? Anemia is having less than normal number of red blood cells or less hemoglobin than normal in the blood. *Microcytic Anemia: Any abnormal.
The Inflammatory Bowel Diseases Crohn’s Disease Ulcerative Colitis Ulceration + granulomas usually in ileum and colon. At risk: Jewish descent; ages
Lower Gastrointestinal disease CELIAC DISEASE LACTOSE INTOLERANCE.
JESSIE BUTTS AMANDA SCHUESSLER Celiac Disease. What is Celiac Disease? Genetically based autoimmune disease  Of all 8 0, only one with a known trigger.
1 Meeting Children’s Special Food and Nutrition Needs in Child Nutrition Programs Lesson 5: Managing Celiac Disease.
CELIAC DISEASE BY EMER BYRNE
Coeliac Disease (CD) By Dr. Zahoor.
Celiac Disease Gluten Sensitive Enteropathy. Celiac Disease: Immune mediated enteropathy caused by permanent sensitivity to gluten in genetically susceptible.
Coeliac Disease. What is Coeliac disease? Autoimmune Heightened immunological response to ingested GLUTEN In genetically susceptible people.
Celiac Sprue Common cause of malabsorption of one or more nutrients in Caucasians, especially those of European descent Also known as non-tropical sprue,
Clinical Approach to Mal digestion & Malabsorption APS.
Bin essa Amer DT204 Presentation on antireticulin antibody.
Gluten...Friend or Foe Presented by Megan, RD. The Rise in Gluten Free Diet Market for gluten free products increased 28% from Americans will.
Celiac Disease: Neurological Manifestations in 2 undiagnosed patients Kogulavadanan Arumaithurai MD, Ashish Kapoor MD, Holli Horak MD, Katalin Scherer.
Lower Gastrointestinal Tract KNH 411. © 2007 Thomson - Wadsworth.
Presented by: Dallas Montag Date: 12/6/16
Gastrointestinal and liver diseases
D- Xylose Absorption Test
Chronic Disease.
Investigating the role of Ca+2/calmodulin dependent kinase pathways
Gastrointestinal and liver diseases
Coeliac Disease at ABCD
Malabsorption syndrome
Gluten and Celiac Disease
Figure 2 Endoscopic imaging of intestinal villi
Malabsorption Syndromes
Chronic Disease.
Chronic Disease.
Lecture 7c 21 October 2016.
Nat. Rev. Gastroenterol. Hepatol. doi: /nrgastro
Fig. 5 Cytosolic delivery of toxic proteins.
Presentation transcript:

NATIONAL RESEARCH & DEVELOPMENT INSTITUTE FOR BIOLOGY AND ANIMAL NUTRITION ROLE OF ENRICHED CALCIUM AND IRON YEASTS IN COELIAC DISEASE MARIN D.E. 1, DUTA D. 2, BARBULESCU D. 2, PISTOL G.C. 1 and I. TARANU 1 1 National Institute for Research and Development for Biology and Animal Nutrition, Laboratory of Animal Biology, Calea Bucuresti, no. 1, Balotesti, Ilfov 2 National Institute for Research and Development for Food Bioresouces, Bucharest, Romania 3 S.C. PharmacorpInnovation, Bucharest, Romania ROLE OF ENRICHED CALCIUM AND IRON YEASTS IN COELIAC DISEASE MARIN D.E. 1, DUTA D. 2, BARBULESCU D. 2, PISTOL G.C. 1 and I. TARANU 1 1 National Institute for Research and Development for Biology and Animal Nutrition, Laboratory of Animal Biology, Calea Bucuresti, no. 1, Balotesti, Ilfov 2 National Institute for Research and Development for Food Bioresouces, Bucharest, Romania 3 S.C. PharmacorpInnovation, Bucharest, Romania Introduction Results and discussion Selected bibliography Material and Methods Conclusions Coeliac disease (CD) is an autoimmune enteropathy manifested in genetically susceptible individuals due to their permanent intolerance to wheat gluten (Sollid et al. 2000). Gluten proteins and their toxic components (gliadins) are partially resistant to proteolytic degradation and can accumulate and interact with the small intestinal mucosa (Hausch et al., 2002). This disease is considered as both a food hypersensitivity and an autoimmune disorder that involves genetic and environmental factors (Sollid and Khosla, 2005). It is characterized by villous atrophy and crypt hyperplasia, primarily in the duodenum and jejunum, with inflammatory changes leading to malabsorption (Gujral et al., 2012). In CD- patients, malabsorption is frequently encountered (McGough et al., 2005) and micronutrient deficiencies may arise (Dickey et al., 2008). For this reason, patients with coeliac disease need vitamin and mineral supplements in addition to a gluten free diet (Malterre, 2009). In the present study, we have analyzed the effect of some bread and vine strains of yeast (Saccharomyces cerevisiae) enriched with minerals (Ca, Fe or both) on human colon carcinoma Caco-2 cell line. 1mg/mL gliadin induced a significant decrease of cell Caco2 cell viability, as resulted from the MTT test.  Gliadin significantly decrease cell viability and transepithelial electrical resistance of the CaCo2 cells.  SC6 - an yeast enriched with iron, (1mg/mL) significantly improve cell viability decreased by gliadin.  SC6 - an yeast enriched with iron and SC8 - an yeast enriched with calcium and iron at the concentration of 1mg/mL significantly improve the transepithelial electrical resistance of the CaCo2 cells.  The use of fermented products fortified with minerals could improve the general health status in CD diagnosed patients. 1.Sollid. L.M Coeliac disease: dissecting a complex inflammatory disorder Nature Reviews Immunology 2, Gujral N, Freeman HJ, Thomson AB Celiac disease: prevalence, diagnosis, pathogenesis and treatment. World J. Gastroenterol. 18(42): McGough N., Cumminigs JH Coeliac disease: a diverse clinical syndrome caused by intolerance of wheat, barley and rye. Proc Nutr Soc. 64(4): Dickey W, Kearney N Overweight in celiac disease: prevalence, clinical characteristics, and effect of a gluten-free diet. Am J Gastroenterol. 101(10): Malterre T Digestive and nutritional considerations in celiac disease: could supplementation help?Altern Med Rev. 14(3): This work was supported by the project PCCA2 no.111/2012 financed by UEFISCDI. Acknowledgments Before treatment, gliadins were subjected to a simulated human gastrointestinal digestion with trypsin and pepsin (Drago et al., 2006). Cells were administered 1mg/mL gliadin and two concentrations of yeasts: 1  g/mL and 1mg/mL, respectively. Cells were cultivated in MEM medium supplemented with 2 mM L-Glu, 100 mg/mL penicillin, 100 mg/mL streptomycin and 20% SFV and treated or not with gliadin and yeasts for 48h (MTT test) or for 21 days (TEER experiments). Optical De nsity (nm) Gliadin (1mg/mL) S. cerevisiae (1  g/mL) Optical Density (nm) Gliadin (1mg/mL) S. cerevisiae (1 m g/mL) SC 2 SC 7 SC 8 SC 6 The eight strains analysed, weren’t able to rehabilitate the cell viability affected by gliadin, when administered at a concentration of 1  g/mL. By contrast at the dose of 1mg/mL, only S. cerevisiae strain (SC6), Fe enriched, was able to rehabilitate the viability of Caco2 cells. 1mg/mL gliadin induce an significant decrease of transepithelial electrical resistance (TEER) as a marker of epithelium integrity, with 22.5 percentage from control. By contrast, in absence of gliadin, the yeast strains did not affect the TEER values as can be seen in the figure 2. SC6 along with another three strains of yeast (enriched in Ca or in both Ca and Fe) were able to improve the TEER values decreased by gliadin. SC6 (Fe enriched), but also SC8 (Ca and Fe enriched) were the most efficient in the restoration of the TER values. * * * TEER (%) * * * Fig. 1 Effect of gliadin and S.cerevisiae yeasts enriched with minerals on cell viability Fig. 2 Effect of gliadin and S.cerevisiae yeasts enriched with minerals on TEER * * * *