Enteropathy induced in young rats by feeding with gliadin--similarity with coeliac disease
Jazyk angličtina Země Česko Médium print
Typ dokumentu časopisecké články
PubMed
2653886
Knihovny.cz E-zdroje
- MeSH
- časové faktory MeSH
- ELISA MeSH
- fluorescenční protilátková technika MeSH
- gliadin krev toxicita MeSH
- imunoglobulin A analýza MeSH
- imunoglobulin G analýza MeSH
- kolika etiologie MeSH
- krysa rodu Rattus MeSH
- nemoci jejuna etiologie imunologie MeSH
- nemoci střev chemicky indukované MeSH
- rostlinné proteiny toxicita MeSH
- věkové faktory MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- gliadin MeSH
- imunoglobulin A MeSH
- imunoglobulin G MeSH
- rostlinné proteiny MeSH
Young rats (10- and 21-day-old) were given gliadin by intragastric application, in the form of a 5% and 0.5% solution. A 5% gliadin (1 ml) was intolerable for young rats, destroying the structure of their jejunal mucosa. A 0.5% gliadin (1 ml) was well tolerated by 21-day-old animals and caused no changes in enterocytes. Repeated administration of 0.5% gliadin on days 0 and 17 caused an increased lymphocyte infiltration in the lamina propria and an increase in the number of cells producing IgA immunoglobulins. Repeated intragastric administration of 0.5% gliadin until 1 month of age, followed by a single administration of 0.5% gliadin at 2 months, caused shortening of the jejunal villi and changes in apical enterocytes. The most pronounced immunological changes were observed in these repeatedly treated animals. Increased numbers of lymphocytes producing IgG in the lamina propria were found and the intestinal contents of these animals exhibited an increased level of IgG and IgA anti-gliadin antibodies when compared to control rats. The results indicate that some morphological and immunological changes observed in young rats fed with gliadin resemble those observed in patients with coeliac disease. The described experimental model is supposed to be suitable for studying the pathogenetic aspects of human coeliac disease.