BACKGROUND: Coeliac disease (CD) or gluten-sensitive enteropathy is a chronic gastrointestinal disease of children and adults. An experimental model using inbred germfree rats has been developed to study the effects of intragastric gliadin application on intestinal mucosa. METHODS: AVN strain Wistar rats (inbred F 87)-germfree were used. Gliadin was applied by intragastric probe from birth until day 63 (0.5-5 mg of gliadin per immunization). Intraepithelial lymphocytes (IEL) were separated from the jejunum, and surface marker characterization was performed using flow cytometry. Isolated IEL were labelled with fluorescein isothiocyanate and injected into control jejunal loops. After 1 h and 6 h the abdominal cavity was reopened. The samples of jejunum were fixed. RESULTS: Prolonged application of gliadin led to the shortening of jejunal villi, crypt hyperplasia, increased number of mitoses in the crypt epithelium, and increased number of IEL-characteristic CD8+, RGL-1+, and TcR alpha/beta +. Transfer of IEL separated from rats fed with gliadin into the intestinal loops of untreated rats led to tight junctions in the enterocytes of the intestinal loops. The IEL isolated from controls (albumin-treated) induced no mucosal changes in intestinal loops. CONCLUSION: These data suggest that IEL isolated from gliadin-treated rats transfer mucosal damage and that gluten-induced enteropathy has an autoimmune component.
BACKGROUND:Coeliac disease (CD) or gluten-sensitive enteropathy is a chronic gastrointestinal disease of children and adults. An experimental model using inbred germfree rats has been developed to study the effects of intragastric gliadin application on intestinal mucosa. METHODS: AVN strain Wistar rats (inbred F 87)-germfree were used. Gliadin was applied by intragastric probe from birth until day 63 (0.5-5 mg of gliadin per immunization). Intraepithelial lymphocytes (IEL) were separated from the jejunum, and surface marker characterization was performed using flow cytometry. Isolated IEL were labelled with fluorescein isothiocyanate and injected into control jejunal loops. After 1 h and 6 h the abdominal cavity was reopened. The samples of jejunum were fixed. RESULTS: Prolonged application of gliadin led to the shortening of jejunal villi, crypt hyperplasia, increased number of mitoses in the crypt epithelium, and increased number of IEL-characteristic CD8+, RGL-1+, and TcR alpha/beta +. Transfer of IEL separated from rats fed with gliadin into the intestinal loops of untreated rats led to tight junctions in the enterocytes of the intestinal loops. The IEL isolated from controls (albumin-treated) induced no mucosal changes in intestinal loops. CONCLUSION: These data suggest that IEL isolated from gliadin-treated rats transfer mucosal damage and that gluten-induced enteropathy has an autoimmune component.
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Authors: Manuel A Silva; Jennifer Jury; Yolanda Sanz; Michelle Wiepjes; Xianxi Huang; Joseph A Murray; Chella S David; Alessio Fasano; Elena F Verdú Journal: Dig Dis Sci Date: 2011-08-07 Impact factor: 3.199
Authors: H Tlaskalová-Hogenová; R Stĕpánková; L Tucková; M A Farré; D P Funda; E F Verdú; J Sinkora; T Hudcovic; Z Reháková; B Cukrowska; H Kozáková; L Prokesová Journal: Folia Microbiol (Praha) Date: 1998 Impact factor: 2.099
Authors: H Kozáková; R Stĕpánková; J Kolínská; M A Farré; D P Funda; L Tucková; H Tlaskalová-Hogenová Journal: Folia Microbiol (Praha) Date: 1998 Impact factor: 2.099
Authors: Heather J Galipeau; Justin L McCarville; Sina Huebener; Owen Litwin; Marlies Meisel; Bana Jabri; Yolanda Sanz; Joseph A Murray; Manel Jordana; Armin Alaedini; Fernando G Chirdo; Elena F Verdu Journal: Am J Pathol Date: 2015-10-09 Impact factor: 4.307