ORIGINAL RESEARCH The Food Additive Maltodextrin Promotes Endoplasmic Reticulum Stress – Driven Q2 Mucus Depletion and Exacerbates Intestinal In fl ammation

This study reports that the polysaccharide maltodextrin, which is a common additive used in Western diet for food processing, triggers endoplasmic reticulum stress in goblet cells. Our data support the hypothesis that a Western diet rich in maltodextrin can contribute to gut disease susceptibility and can help Q8 design preventive programs for subjects at high risk to develop in fl ammatory bowel diseases. BACKGROUND stabilizers,

[1]  Kai Huang,et al.  Tauroursodeoxycholic acid inhibits intestinal inflammation and barrier disruption in mice with non‐alcoholic fatty liver disease , 2017, British journal of pharmacology.

[2]  R. Sartor,et al.  Dietary Salt Exacerbates Experimental Colitis , 2017, The Journal of Immunology.

[3]  M. Marzorati,et al.  Dietary emulsifiers directly alter human microbiota composition and gene expression ex vivo potentiating intestinal inflammation , 2017, Gut.

[4]  I. Monteleone,et al.  Sodium chloride–enriched Diet Enhanced Inflammatory Cytokine Production and Exacerbated Experimental Colitis in Mice , 2017, Journal of Crohn's & colitis.

[5]  P. Wilmes,et al.  A Dietary Fiber-Deprived Gut Microbiota Degrades the Colonic Mucus Barrier and Enhances Pathogen Susceptibility , 2016, Cell.

[6]  A. Perkins,et al.  High Fat Diets Induce Colonic Epithelial Cell Stress and Inflammation that is Reversed by IL-22 , 2016, Scientific Reports.

[7]  G. Rogler,et al.  Titanium dioxide nanoparticles exacerbate DSS-induced colitis: role of the NLRP3 inflammasome , 2016, Gut.

[8]  F. Clavel-Chapelon,et al.  Dietary Patterns and Risk of Inflammatory Bowel Disease in Europe: Results from the EPIC Study , 2016, Inflammatory bowel diseases.

[9]  A. Ananthakrishnan,et al.  Measures of Obesity and Risk of Crohn's Disease and Ulcerative Colitis , 2015, Inflammatory bowel diseases.

[10]  Omry Koren,et al.  Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome , 2015, Nature.

[11]  E. Segal,et al.  Artificial sweeteners induce glucose intolerance by altering the gut microbiota , 2014, Nature.

[12]  C. A. de la Motte,et al.  The Dietary Polysaccharide Maltodextrin Promotes Salmonella Survival and Mucosal Colonization in Mice , 2014, PloS one.

[13]  G. Calamita,et al.  High-fat diet alters the oligosaccharide chains of colon mucins in mice , 2014, Histochemistry and Cell Biology.

[14]  W. Willett,et al.  Long-term intake of dietary fat and risk of ulcerative colitis and Crohn's disease , 2013, Gut.

[15]  S. Sarker.  Faculty Opinions recommendation of Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10-/- mice. , 2013 .

[16]  N. Barnich,et al.  Western diet induces dysbiosis with increased E coli in CEABAC10 mice, alters host barrier function favouring AIEC colonisation , 2013, Gut.

[17]  M. Johansson,et al.  The gastrointestinal mucus system in health and disease , 2013, Nature Reviews Gastroenterology &Hepatology.

[18]  F. Moreau,et al.  Entamoeba histolytica exacerbates epithelial tight junction permeability and proinflammatory responses in Muc2(-/-) mice. , 2013, The American journal of pathology.

[19]  A. Gewirtz,et al.  Bacteria penetrate the normally impenetrable inner colon mucus layer in both murine colitis models and patients with ulcerative colitis , 2013, Gut.

[20]  D. Ron,et al.  Negative feedback by IRE1β optimizes mucin production in goblet cells , 2013, Proceedings of the National Academy of Sciences.

[21]  C. McDonald,et al.  Crohn's Disease-Associated Adherent-Invasive Escherichia coli Adhesion Is Enhanced by Exposure to the Ubiquitous Dietary Polysaccharide Maltodextrin , 2012, PloS one.

[22]  D. Ron,et al.  The ER stress transducer IRE1β is required for airway epithelial mucin production , 2012, Mucosal Immunology.

[23]  M. Federici,et al.  Tissue inhibitor of metalloproteinase-3 regulates inflammation in human and mouse intestine. , 2012, Gastroenterology.

[24]  A. Young,et al.  Fecal Lipocalin 2, a Sensitive and Broadly Dynamic Non-Invasive Biomarker for Intestinal Inflammation , 2012, PloS one.

[25]  K. Hemminki,et al.  Risk of inflammatory bowel disease in first‐ and second‐generation immigrants in Sweden: A nationwide follow‐up study , 2011, Inflammatory bowel diseases.

[26]  G. Radford-Smith,et al.  An intestinal epithelial defect conferring ER stress results in inflammation involving both innate and adaptive immunity , 2010, Mucosal Immunology.

[27]  Gunnar C. Hansson,et al.  The two mucus layers of colon are organized by the MUC2 mucin, whereas the outer layer is a legislator of host–microbial interactions , 2010, Proceedings of the National Academy of Sciences.

[28]  B. Finlay,et al.  Muc2 Protects against Lethal Infectious Colitis by Disassociating Pathogenic and Commensal Bacteria from the Colonic Mucosa , 2010, PLoS pathogens.

[29]  B. Stoll,et al.  Carbohydrate maldigestion induces necrotizing enterocolitis in preterm pigs. , 2009, American journal of physiology. Gastrointestinal and liver physiology.

[30]  V. Loening-Baucke,et al.  Bacterial Overgrowth and Inflammation of Small Intestine After Carboxymethylcellulose Ingestion in Genetically Susceptible Mice , 2009, Inflammatory bowel diseases.

[31]  A. Velcich,et al.  The inner of the two Muc2 mucin-dependent mucus layers in colon is devoid of bacteria , 2008, Proceedings of the National Academy of Sciences.

[32]  C. Goodnow,et al.  Aberrant Mucin Assembly in Mice Causes Endoplasmic Reticulum Stress and Spontaneous Inflammation Resembling Ulcerative Colitis , 2008, PLoS medicine.

[33]  J. Meijerink,et al.  Muc2-deficient mice spontaneously develop colitis, indicating that MUC2 is critical for colonic protection. , 2006, Gastroenterology.

[34]  Li-Xia Guo,et al.  Differential phosphorylation of p38 induced by apoptotic and anti-apoptotic stimuli in murine hepatocytes. , 2005, World journal of gastroenterology.

[35]  Y. Tabuchi,et al.  Therapeutic potential of follistatin for colonic inflammation in mice. , 2005, Gastroenterology.

[36]  G. Bouma,et al.  The immunological and genetic basis of inflammatory bowel disease , 2003, Nature Reviews Immunology.

[37]  Kan Yang,et al.  Colorectal Cancer in Mice Genetically Deficient in the Mucin Muc2 , 2002, Science.

[38]  S. Yamato,et al.  Epidemiologic analysis of Crohn disease in Japan: increased dietary intake of n-6 polyunsaturated fatty acids and animal protein relates to the increased incidence of Crohn disease in Japan. , 1996, The American journal of clinical nutrition.

[39]  John C. Lee,et al.  Role of CSBP/p38/RK stress response kinase in LPS and cytokine signaling mechanisms , 1996, Journal of leukocyte biology.

[40]  L Bibbs,et al.  A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells. , 1994, Science.

[41]  A. Yamauchi,et al.  Mitogen-activated protein kinase and its activator are regulated by hypertonic stress in Madin-Darby canine kidney cells. , 1994, The Journal of clinical investigation.

[42]  J. Thompson,et al.  Prevalence and family risk of ulcerative colitis and Crohn's disease: an epidemiological study among Europeans and south Asians in Leicestershire. , 1993, Gut.

[43]  J. Lewis,et al.  Diet as a Trigger or Therapy for Inflammatory Bowel Diseases. , 2017, Gastroenterology.

[44]  J. Bornstein,et al.  Alterations of colonic function in the Winnie mouse model of spontaneous chronic colitis. , 2017, American journal of physiology. Gastrointestinal and liver physiology.

[45]  Judy H. Cho.  Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease , 2016 .

[46]  Subrata Ghosh,et al.  Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. , 2012, Gastroenterology.

[47]  E. Szigethy,et al.  Inflammatory bowel disease. , 2011, Pediatric clinics of North America.

[48]  Chih‐Chung Lin,et al.  Interleukin-1beta induces MMP-9 expression via p42/p44 MAPK, p38 MAPK, JNK, and nuclear factor-kappaB signaling pathways in human tracheal smooth muscle cells. , 2007, Journal of cellular physiology.

[49]  P. Geiger,et al.  Activation of p38 MAP kinase enhances sensitivity of muscle glucose transport to insulin. , 2005, American journal of physiology. Endocrinology and metabolism.