Background information: Celiac disease is a chronic inflammatory disorder of the small bowel induced in genetically susceptible subjects by gluten ingestion. Diarrhea, weight loss and malabsorption represent the major clinical presentation of the disease. Here we examined the possible alteration in the expression and localization of water channels (aquaporins) and some solute transporters in duodenal mucosa of celiac disease patients. Duodenal biopsies from untreated celiacs, treated celiacs, healthy controls and disease controls were considered in this investigation. The expression of some aquaporins and transporters mRNA in human duodenal biopsies was determined by semi-quantitative RT-PCR and real time RT-PCR. The localization of aquaporin 3, 7 and 10, and of Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger was evaluated by immunohistochemistry. Results: Aquaporin 3, 7, 10, 11, Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger, cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter mRNAs were expressed in duodenal biopsies of healthy controls, treated celiac patients and disease controls. The expression of transcripts was virtually absent in duodenal biopsies of untreated celiac disease patients except for cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter. In healthy controls immunohistochemistry revealed a labeling in the apical membrane of surface epithelial cells of duodenum. The immunolabeling resulted heavily reduced or absent in untreated celiac patients while it was normal in patients consuming gluten free diet for at least 12 months. Conclusions: Our results indicate that the main routes for water and solute absorption are deficient in celiac disease and may play a role in malabsorption symptoms onset.
Solute transporters and aquaporins are impaired in celiac disease / U. Laforenza, E. Miceli, G. Gastaldi, M.F. Scaffino, U. Ventura, J.M. Fontana, M.N. Orsenigo, G.R. Corazza. - In: BIOLOGY OF THE CELL. - ISSN 0248-4900. - 102:8(2010), pp. 457-467. [10.1042/BC20100023]
Solute transporters and aquaporins are impaired in celiac disease
M.N. OrsenigoPenultimo
;
2010
Abstract
Background information: Celiac disease is a chronic inflammatory disorder of the small bowel induced in genetically susceptible subjects by gluten ingestion. Diarrhea, weight loss and malabsorption represent the major clinical presentation of the disease. Here we examined the possible alteration in the expression and localization of water channels (aquaporins) and some solute transporters in duodenal mucosa of celiac disease patients. Duodenal biopsies from untreated celiacs, treated celiacs, healthy controls and disease controls were considered in this investigation. The expression of some aquaporins and transporters mRNA in human duodenal biopsies was determined by semi-quantitative RT-PCR and real time RT-PCR. The localization of aquaporin 3, 7 and 10, and of Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger was evaluated by immunohistochemistry. Results: Aquaporin 3, 7, 10, 11, Na+/glucose cotransporter, H+/oligopeptide transporter and Na+/H+ exchanger, cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter mRNAs were expressed in duodenal biopsies of healthy controls, treated celiac patients and disease controls. The expression of transcripts was virtually absent in duodenal biopsies of untreated celiac disease patients except for cystic fibrosis transmembrane conductance regulator and Na-K-2Cl cotransporter. In healthy controls immunohistochemistry revealed a labeling in the apical membrane of surface epithelial cells of duodenum. The immunolabeling resulted heavily reduced or absent in untreated celiac patients while it was normal in patients consuming gluten free diet for at least 12 months. Conclusions: Our results indicate that the main routes for water and solute absorption are deficient in celiac disease and may play a role in malabsorption symptoms onset.Pubblicazioni consigliate
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