Eur J Gastroenterol Hepatol 2009 Jul;21(7):794-804
Institute for Cancer Studies, University of Birmingham Cancer Research, UK.
Background: Sixty percent of people with coeliac disease (CD) are iron deficient. Many, however, remain iron replete despite the disease.
Aims: (i) To characterize the changes in duodenal iron transport proteins in CD with and without iron deficiency. (ii) To examine if iron-activated gut lymphocytes can inhibit iron export in an enterocyte cell model.
Methods: Endoscopic duodenal biopsies were collected from patients with normal duodenum with and without iron deficiency anaemia and untreated CD sufferers with iron deficiency (n=10 each group). mRNA expression of iron transport proteins was determined by quantitative real time PCR. Protein localization and expression was determined from histology sections in patients with normal duodenum (n=20), and patients with untreated CD with and without iron deficiency (n=20). In addition, CaCo2 cells were cocultured with iron-activated lymphocytes 55Fe was used to determine the effect on CaCo2 cell iron transport.
Results: The expression of divalent metal transporter 1 and ferroportin was increased in CD with or without iron deficiency. Ferritin expression was increased in CD but only in those with associated iron deficiency. TNF-alpha produced by activated lymphocytes inhibited iron export from CaCo2 cells.
Conclusion: Increased enterocyte ferritin expression may promote iron deficiency in CD and this effect seems to be dependent upon TNF-alpha expression in gut lymphocytes.